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Volume 33,Issue 4,2026 Table of Contents
2026, 33(4):351-362.
Abstract:
[Abstract] Colorectal cancer (CRC), a malignant tumor, is a leading cause of cancer-related morbidity and mortality worldwide. Accumulating evidence suggests that CRC occurrence and development are closely associated not only with intestinal microbiota dysbiosis, but also with oral microbiota. Specific oral microbes can translocate via the oral-gut axis to colonize the intestinal tract and distant tumor sites. Through mechanisms such as adhesion and colonization, activation of oncogenic signaling pathways, enhancement of tumor cell migration and invasion, and remodeling of the tumor microenvironment, these microbes promote tumor progression and may influence responses to anticancer therapies. These findings highlight the potential of targeting oral microbiota in CRC clinical management. This review systematically summarizes the molecular mechanisms by which oral microbiota contributes to CRC pathogenesis, with a particular focus on microbial intervention strategies that target the oral-gut axis. This review also discusses current research limitations and future directions, aiming to provide a reference for both basic research and clinical translation in this field.
[Abstract] Colorectal cancer (CRC), a malignant tumor, is a leading cause of cancer-related morbidity and mortality worldwide. Accumulating evidence suggests that CRC occurrence and development are closely associated not only with intestinal microbiota dysbiosis, but also with oral microbiota. Specific oral microbes can translocate via the oral-gut axis to colonize the intestinal tract and distant tumor sites. Through mechanisms such as adhesion and colonization, activation of oncogenic signaling pathways, enhancement of tumor cell migration and invasion, and remodeling of the tumor microenvironment, these microbes promote tumor progression and may influence responses to anticancer therapies. These findings highlight the potential of targeting oral microbiota in CRC clinical management. This review systematically summarizes the molecular mechanisms by which oral microbiota contributes to CRC pathogenesis, with a particular focus on microbial intervention strategies that target the oral-gut axis. This review also discusses current research limitations and future directions, aiming to provide a reference for both basic research and clinical translation in this field.
ZOU Huangren
,
LIU Yanlin
,
ZHANG Lu
,
BAI Yuke
,
GAO Rui
,
QIN Tiantian
,
FANG Ruotong
,
DENG Ziyong
2026, 33(4):363-372.
Abstract:
[Abstract] Objective: To investigate the mechanism by which lncRNA DLEU2 regulates IKKα-mediated radioiodine resistance in thyroid carcinoma (TC) through the EZH2/H3K27me3 axis. Methods: DLEU2 expression and its association with EZH2 in TC were analyzed using the TCGA database. Radioiodine-resistant TPC-1 cell (RR-TPC-1 cell) model and the nude mouse xenograft models were established. Following interventions including DLEU2 knockdown or overexpression (si-DLEU2/OE-DLEU2), EZH2 inhibition (UNC1999), and IKKα overexpression (OE-IKKα), gene and protein expression, histone modifications, cell proliferation, apoptosis, and tumorigenicity were detected by qPCR, Western blot, RNA immunoprecipitation (RIP), chromatin immunoprecipitation (ChIP), CCK-8 assay, flow cytometry, TUNEL staining, and xenograft tumor growth assay. Results: TCGA analysis revealed significant upregulation of DLEU2 in TC (P < 0.001), which was associated with poor prognosis (P = 0.0084) and was positively correlated with EZH2 expression (Pearson r = 0.390, P < 0.001). RIP assay revealed an interaction between EZH2 and DLEU2 (P < 0.05). In vitro experiments indicated that DLEU2 knockdown in RR-TPC-1 cells markedly reduced EZH2 and IKKα expression as well as H3K27me3 levels, inhibited NF-κB pathway activation (P < 0.05 or P < 0.01), suppressed cell proliferation and promoted cell apoptosis (all P < 0.05). DLEU2 knockdown combined with EZH2 inhibition further enhanced these effects while IKKα overexpression partially reversed these effects (P < 0.05 or P < 0.01). In vivo experiments further demonstrated that DLEU2 knockdown combined with EZH2 inhibition significantly inhibited xenograft growth and promoted tumor cell apoptosis (all P < 0.01), while IKKα overexpression partially reversed the above-mentioned anti-tumor effects (P < 0.05 or P < 0.01). Conclusion: lncRNA DLEU2, through recruiting EZH2 to catalyze H3K27me3 modification, indirectly activates the IKKα/NF-κB signaling and establishes a positive feedback loop, which mediates 131I resistance in TPC-1 cells.
[Abstract] Objective: To investigate the mechanism by which lncRNA DLEU2 regulates IKKα-mediated radioiodine resistance in thyroid carcinoma (TC) through the EZH2/H3K27me3 axis. Methods: DLEU2 expression and its association with EZH2 in TC were analyzed using the TCGA database. Radioiodine-resistant TPC-1 cell (RR-TPC-1 cell) model and the nude mouse xenograft models were established. Following interventions including DLEU2 knockdown or overexpression (si-DLEU2/OE-DLEU2), EZH2 inhibition (UNC1999), and IKKα overexpression (OE-IKKα), gene and protein expression, histone modifications, cell proliferation, apoptosis, and tumorigenicity were detected by qPCR, Western blot, RNA immunoprecipitation (RIP), chromatin immunoprecipitation (ChIP), CCK-8 assay, flow cytometry, TUNEL staining, and xenograft tumor growth assay. Results: TCGA analysis revealed significant upregulation of DLEU2 in TC (P < 0.001), which was associated with poor prognosis (P = 0.0084) and was positively correlated with EZH2 expression (Pearson r = 0.390, P < 0.001). RIP assay revealed an interaction between EZH2 and DLEU2 (P < 0.05). In vitro experiments indicated that DLEU2 knockdown in RR-TPC-1 cells markedly reduced EZH2 and IKKα expression as well as H3K27me3 levels, inhibited NF-κB pathway activation (P < 0.05 or P < 0.01), suppressed cell proliferation and promoted cell apoptosis (all P < 0.05). DLEU2 knockdown combined with EZH2 inhibition further enhanced these effects while IKKα overexpression partially reversed these effects (P < 0.05 or P < 0.01). In vivo experiments further demonstrated that DLEU2 knockdown combined with EZH2 inhibition significantly inhibited xenograft growth and promoted tumor cell apoptosis (all P < 0.01), while IKKα overexpression partially reversed the above-mentioned anti-tumor effects (P < 0.05 or P < 0.01). Conclusion: lncRNA DLEU2, through recruiting EZH2 to catalyze H3K27me3 modification, indirectly activates the IKKα/NF-κB signaling and establishes a positive feedback loop, which mediates 131I resistance in TPC-1 cells.
2026, 33(4):373-378.
Abstract:
[Abstract] Objective: To investigate the regulatory effect of bufalin (BU) on tumor-associated macrophage (TAM)-mediated programmed death-ligand 1 (PD-L1) expression in colorectal cancer (CRC) cells and to elucidate the underlying molecular mechanism. Methods: An in vitro co-culture system was established using HCT116 cells and THP-1-derived macrophages. THP-1 cells were differentiated into M0 macrophages by PMA treatment and further stimulated with HCT116-conditioned medium (CM) to generate TAM-like cells. Flow cytometry was used to detect CD11b and CD206 expressions and assess macrophage polarization level. The changes in the expression levels of TGF-β, IL-10, STAT3/p-STAT3, and PD-L1 were detected by RT-qPCR and WB assay. A STAT3 knockdown cell line (HCT116-shSTAT3), constructed by lentiviral transduction, was combined with BU treatment to verify the role of the STAT3/PD-L1 signaling pathway. Results: HCT116-derived CM induced macrophage polarization toward the M2 phenotype, as evidenced by an increased proportion of CD11b+CD206+ cells (P < 0.01) and elevated expression of TGF-β and IL-10 (both P < 0.001). TAM-conditioned medium significantly promoted STAT3 phosphorylation (P < 0.001) and upregulated PD-L1 expression at both mRNA and protein levels in HCT116 cells (P < 0.001 or P < 0.01). BU treatment markedly suppressed TAM-mediated STAT3 phosphorylation and concomitantly reduced PD-L1 expression (both P < 0.01). STAT3 knockdown decreased PD-L1 expression, with a trend consistent with BU treatment. Conclusion: BU can downregulate PD-L1 expression in CRC cells by inhibiting TAM-mediated STAT3 signaling activation, suggesting its potential application value in the tumor immune microenvironment.
[Abstract] Objective: To investigate the regulatory effect of bufalin (BU) on tumor-associated macrophage (TAM)-mediated programmed death-ligand 1 (PD-L1) expression in colorectal cancer (CRC) cells and to elucidate the underlying molecular mechanism. Methods: An in vitro co-culture system was established using HCT116 cells and THP-1-derived macrophages. THP-1 cells were differentiated into M0 macrophages by PMA treatment and further stimulated with HCT116-conditioned medium (CM) to generate TAM-like cells. Flow cytometry was used to detect CD11b and CD206 expressions and assess macrophage polarization level. The changes in the expression levels of TGF-β, IL-10, STAT3/p-STAT3, and PD-L1 were detected by RT-qPCR and WB assay. A STAT3 knockdown cell line (HCT116-shSTAT3), constructed by lentiviral transduction, was combined with BU treatment to verify the role of the STAT3/PD-L1 signaling pathway. Results: HCT116-derived CM induced macrophage polarization toward the M2 phenotype, as evidenced by an increased proportion of CD11b+CD206+ cells (P < 0.01) and elevated expression of TGF-β and IL-10 (both P < 0.001). TAM-conditioned medium significantly promoted STAT3 phosphorylation (P < 0.001) and upregulated PD-L1 expression at both mRNA and protein levels in HCT116 cells (P < 0.001 or P < 0.01). BU treatment markedly suppressed TAM-mediated STAT3 phosphorylation and concomitantly reduced PD-L1 expression (both P < 0.01). STAT3 knockdown decreased PD-L1 expression, with a trend consistent with BU treatment. Conclusion: BU can downregulate PD-L1 expression in CRC cells by inhibiting TAM-mediated STAT3 signaling activation, suggesting its potential application value in the tumor immune microenvironment.
2026, 33(4):379-388.
Abstract:
[Abstract] Objective: To investigate the transcriptional regulation of HOXD11 (homeobox D11) on Ki-67, its effects on the malignant biological behavior of laryngeal squamous cell carcinoma (LSCC) cells and the underlying mechanisms. Methods: High-throughput sequencing data from GEO and UALCAN databases were used to analyze the differential expression of HOXD11 in LSCC. Tumor and adjacent tissue specimens from 60 patients with LSCC surgically resected at the 980 Hospital of the Joint Logistics Support Force between January 2022 and January 2025, along with human LSCC cell lines AMC-HN-8, TU-177, TU-686, and human normal laryngeal epithelial cells (HNLC) were collected. Cell lines with stable HOXD11 knockdown or overexpression were established, and the cells were divided into the control group, the HOXD11 knockdown group, and the HOXD11 overexpression group. The mRNA expression levels of HOXD11 and Ki-67 genes in LSCC tissues and cells were detected by RT-qPCR. The protein expression and distribution of HOXD11 and Ki-67 in LSCC tissues were analyzed by immunohistochemistry (IHC). Western blot (WB) further verified protein differential expression. MTS, clonogenic assay and Transwell assay were used to detect the effects of HOXD11 knockdown or overexpression on the proliferation, migration and invasion of LSCC cells. Dual luciferase reporter gene experiment and ChIP experiment were used to confirm the regulatory effect of HOXD11 on Ki-67 promoter activity. Results: GEO and UALCAN database analyses showed that HOXD11 was highly expressed in LSCC (P < 0.01). The expressions of HOXD11 and Ki-67 mRNA in LSCC tissues were significantly higher than those in adjacent tissues (both P < 0.01). At the same time, there was a positive correlation between the expressions of HOXD11 and Ki-67 mRNA (r = 0.26, P < 0.05). The expressions of HOXD11 mRNA in LSCC cell lines were significantly higher than those in HNLC (all P < 0.01). HOXD11 knockdown significantly inhibited the proliferation, migration and invasion of LSCC cells (all P < 0.01), while HOXD11 overexpression promoted these malignant biological behaviors of LSCC cells (all P < 0.01). Both dual-luciferase reporter gene assay and ChIP assay confirmed that HOXD11 could directly bind to the Ki-67 promoter region to regulate its expression (P < 0.01). The rescue experiment showed that overexpression of Ki-67 partially reversed the inhibitory effect of HOXD11 knockdown on the proliferation, migration and invasion of LSCC cells (all P < 0.01). Conclusion: HOXD11 is highly expressed in LSCC tissues and cell lines. It directly regulates Ki-67 transcriptional activity and promotes the proliferation, migration and invasion of LSCC cells.
[Abstract] Objective: To investigate the transcriptional regulation of HOXD11 (homeobox D11) on Ki-67, its effects on the malignant biological behavior of laryngeal squamous cell carcinoma (LSCC) cells and the underlying mechanisms. Methods: High-throughput sequencing data from GEO and UALCAN databases were used to analyze the differential expression of HOXD11 in LSCC. Tumor and adjacent tissue specimens from 60 patients with LSCC surgically resected at the 980 Hospital of the Joint Logistics Support Force between January 2022 and January 2025, along with human LSCC cell lines AMC-HN-8, TU-177, TU-686, and human normal laryngeal epithelial cells (HNLC) were collected. Cell lines with stable HOXD11 knockdown or overexpression were established, and the cells were divided into the control group, the HOXD11 knockdown group, and the HOXD11 overexpression group. The mRNA expression levels of HOXD11 and Ki-67 genes in LSCC tissues and cells were detected by RT-qPCR. The protein expression and distribution of HOXD11 and Ki-67 in LSCC tissues were analyzed by immunohistochemistry (IHC). Western blot (WB) further verified protein differential expression. MTS, clonogenic assay and Transwell assay were used to detect the effects of HOXD11 knockdown or overexpression on the proliferation, migration and invasion of LSCC cells. Dual luciferase reporter gene experiment and ChIP experiment were used to confirm the regulatory effect of HOXD11 on Ki-67 promoter activity. Results: GEO and UALCAN database analyses showed that HOXD11 was highly expressed in LSCC (P < 0.01). The expressions of HOXD11 and Ki-67 mRNA in LSCC tissues were significantly higher than those in adjacent tissues (both P < 0.01). At the same time, there was a positive correlation between the expressions of HOXD11 and Ki-67 mRNA (r = 0.26, P < 0.05). The expressions of HOXD11 mRNA in LSCC cell lines were significantly higher than those in HNLC (all P < 0.01). HOXD11 knockdown significantly inhibited the proliferation, migration and invasion of LSCC cells (all P < 0.01), while HOXD11 overexpression promoted these malignant biological behaviors of LSCC cells (all P < 0.01). Both dual-luciferase reporter gene assay and ChIP assay confirmed that HOXD11 could directly bind to the Ki-67 promoter region to regulate its expression (P < 0.01). The rescue experiment showed that overexpression of Ki-67 partially reversed the inhibitory effect of HOXD11 knockdown on the proliferation, migration and invasion of LSCC cells (all P < 0.01). Conclusion: HOXD11 is highly expressed in LSCC tissues and cell lines. It directly regulates Ki-67 transcriptional activity and promotes the proliferation, migration and invasion of LSCC cells.
2026, 33(4):389-399.
Abstract:
[Abstract] Objective: To investigate the role and mechanism of the group II innate lymphoid cell (ILC2)-amphiregulin (AREG)-regulatory T (Treg) cell axis in the regulation of the immune microenvironment in cervical cancer. Methods: Tumor tissue samples were obtained from patients with stage I-IIA cervical cancer (n = 8) who were admitted to the First Affiliated Hospital of Xinjiang Medical University between May 2021 and May 2022. Normal cervical tissues from patients undergoing surgery for uterine fibroids served as controls (n = 8). Additionally, peripheral blood samples were collected from patients with cervical cancer at all stages (n = 30), with peripheral blood from healthy individuals serving as controls (n = 30). The mRNA expression levels of AREG and forkhead box protein P3 (Foxp3) were analyzed via the GEPIA database. Multiplex immunofluorescence and flow cytometry were performed to detect the infiltration of ILC2s and Treg cells in tissues and peripheral blood. ELISA, immunohistochemistry (IHC) and WB were carried out to verify the expression of AREG, Foxp3 and IL-10, followed by correlation analysis among ILC2s, AREG, Treg cells and IL-10. For in vitro experiments, ILC2s and peripheral blood mononuclear cells (PBMC) were isolated from cervical cancer patients and treated with recombinant human IL-33 (rhIL-33), anti-IL-33 antibody (α-IL-33), recombinant human AREG (rhAREG) and anti-human AREG antibody (α-AREG), respectively. CCK-8 assay and flow cytometry were used to evaluate the effects of different concentrations of rhAREG on the proliferation and apoptosis of HeLa and SiHa cells. The concentrations of AREG and IL-10 in cell culture supernatants were measured by ELISA, and the proportion of Treg cells were determined by flow cytometry. In addition, this study also compared the differences in the levels of ILC2s, AREG, Treg cells, and IL-10 in the peripheral blood of cervical cancer patients before and after surgery. Results: The infiltration of ILC2 and expression of AREG in tissues and peripheral blood of cervical cancer patients were markedly higher than those in the normal control group. The proportion of Treg cells and expression levels of Foxp3 and IL-10 were also significantly upregulated in cervical cancer patients (P < 0.05). Correlation analysis confirmed a positive correlation among ILC2s, AREG, Treg cells and IL-10. In vitro experiments showed that different concentrations of rhAREG had no significant effects on the proliferation or apoptosis of HeLa and SiHa cells (P > 0.05). rhIL-33 effectively activated ILC2s and upregulated AREG secretion (P < 0.01), which was reversed by α-IL-33 treatment (P < 0.05). rhAREG significantly promoted Treg cell differentiation and IL-10 secretion (P < 0.001), whereas α-AREG markedly reversed these biological effects (P < 0.01). In addition, the levels of ILC2s, Treg cells, AREG and IL-10 in peripheral blood of cervical cancer patients were significantly decreased after surgery (P < 0.0001). Conclusion: The aberrant activation of the ILC2-AREG-Treg immunoregulatory axis may participate in cervical cancer progression by shaping an immunosuppressive tumor microenvironment.
[Abstract] Objective: To investigate the role and mechanism of the group II innate lymphoid cell (ILC2)-amphiregulin (AREG)-regulatory T (Treg) cell axis in the regulation of the immune microenvironment in cervical cancer. Methods: Tumor tissue samples were obtained from patients with stage I-IIA cervical cancer (n = 8) who were admitted to the First Affiliated Hospital of Xinjiang Medical University between May 2021 and May 2022. Normal cervical tissues from patients undergoing surgery for uterine fibroids served as controls (n = 8). Additionally, peripheral blood samples were collected from patients with cervical cancer at all stages (n = 30), with peripheral blood from healthy individuals serving as controls (n = 30). The mRNA expression levels of AREG and forkhead box protein P3 (Foxp3) were analyzed via the GEPIA database. Multiplex immunofluorescence and flow cytometry were performed to detect the infiltration of ILC2s and Treg cells in tissues and peripheral blood. ELISA, immunohistochemistry (IHC) and WB were carried out to verify the expression of AREG, Foxp3 and IL-10, followed by correlation analysis among ILC2s, AREG, Treg cells and IL-10. For in vitro experiments, ILC2s and peripheral blood mononuclear cells (PBMC) were isolated from cervical cancer patients and treated with recombinant human IL-33 (rhIL-33), anti-IL-33 antibody (α-IL-33), recombinant human AREG (rhAREG) and anti-human AREG antibody (α-AREG), respectively. CCK-8 assay and flow cytometry were used to evaluate the effects of different concentrations of rhAREG on the proliferation and apoptosis of HeLa and SiHa cells. The concentrations of AREG and IL-10 in cell culture supernatants were measured by ELISA, and the proportion of Treg cells were determined by flow cytometry. In addition, this study also compared the differences in the levels of ILC2s, AREG, Treg cells, and IL-10 in the peripheral blood of cervical cancer patients before and after surgery. Results: The infiltration of ILC2 and expression of AREG in tissues and peripheral blood of cervical cancer patients were markedly higher than those in the normal control group. The proportion of Treg cells and expression levels of Foxp3 and IL-10 were also significantly upregulated in cervical cancer patients (P < 0.05). Correlation analysis confirmed a positive correlation among ILC2s, AREG, Treg cells and IL-10. In vitro experiments showed that different concentrations of rhAREG had no significant effects on the proliferation or apoptosis of HeLa and SiHa cells (P > 0.05). rhIL-33 effectively activated ILC2s and upregulated AREG secretion (P < 0.01), which was reversed by α-IL-33 treatment (P < 0.05). rhAREG significantly promoted Treg cell differentiation and IL-10 secretion (P < 0.001), whereas α-AREG markedly reversed these biological effects (P < 0.01). In addition, the levels of ILC2s, Treg cells, AREG and IL-10 in peripheral blood of cervical cancer patients were significantly decreased after surgery (P < 0.0001). Conclusion: The aberrant activation of the ILC2-AREG-Treg immunoregulatory axis may participate in cervical cancer progression by shaping an immunosuppressive tumor microenvironment.
2026, 33(4):400-407.
Abstract:
[Abstract] Objective: To explore the effects and mechanisms by which lncRNA nuclear enriched transcript 1 (NEAT1) regulating the miR-1287-5p/DNA damage inducible transcript 4 (DDIT4) axis on the proliferation, apoptosis and invasion of ovarian cancer SKOV3 cells. Methods: Tissue samples of cancer and adjacent tissues from 27 patients with ovarian cancer who underwent surgery at Suizhou Hospital Affiliated to Hubei University of Medicine between June 2023 and June 2024 were collected. Normal human ovarian epithelial cells IOSE80 and ovarian cancer cells SKOV3, CAOV3 and A2780 were also collected. RT-qPCR was used to detect the expressions of lncRNA NEAT1, miR-1287-5p and DDIT4 mRNA in ovarian cancer tissues and cells. SKOV3 cells were divided into the Ctrl group, the si-NC group, the si-NEAT1 group, the si-NEAT1 + anti-miR-NC group, the si-NEAT1 + anti-miR-1287-5p group, the si-NEAT1 + vector group, and the si-NEAT1 + OE-DDIT4 group. The CCK-8 assay, colony formation assay, flow cytometry, and Transwell assay were used to detect the proliferation, apoptosis, and invasion abilities of cells in each group. The WB method was used to detect the protein levels of DDIT4, cyclin D1, p53, and migration-invasion enhancer 1 (MIEN1) in the cells. The dual-luciferase reporter gene was used to verify the targeted binding relationship between lncRNA NEAT1 and miR-1287-5p/DDIT4. The RNA pull-down experiment and RNA immunoprecipitation experiment were used respectively to verify the target binding relationships between lncRNA NEAT1 and miR-1287-5p, and between miR-1287-5p and DDIT4. Additionally, the pcDNA group (transfected with empty vector pcDNA3.1) and the pc-NEAT1 group (transfected with pcDNA-NEAT1) were established to validate the overexpression effects of NEAT1. Results: The expression levels of lncRNA NEAT1 and DDIT4 mRNA in ovarian cancer tissues were significantly higher than those in adjacent tissues (P < 0.05), while the expression level of miR-1287-5p was significantly lower than that in adjacent tissues (P < 0.05). After knockdown of lncRNA NEAT1, compared with those in the Ctrl group and the si-NC group, the expressions of lncRNA NEAT1 and DDIT4 mRNA, the number of colony formation, the cell proliferation activity, the number of cell invasion, and the expressions of DDIT4, cyclin D1, and MIEN1 proteins in the si-NEAT1 group all decreased significantly (all P < 0.05), while the expression of miR-1287-5p, the apoptosis rate, and the expression of p53 protein increased significantly (all P < 0.05). Conversely, overexpression of lncRNA NEAT1 decreased miR-1287-5p expression and increased DDIT4 expression, showing opposite regulatory effects to the knockdown experiment. Further experiments proved that anti-miR-1287-5p or OE-DDIT4 might weaken the inhibitory effect of si-NEAT1 on the proliferation and invasion of SKOV3 cells, as well as its promoting effect on cell apoptosis. lncRNA NEAT1 targetedly regulates miR-1287-5p/DDIT4. Conclusion: lncRNA NEAT1 enhances SKOV3 cell proliferation and invasion, and inhibits cell apoptosis by targeting regulating the miR-1287-5p/DDIT4 axis.
[Abstract] Objective: To explore the effects and mechanisms by which lncRNA nuclear enriched transcript 1 (NEAT1) regulating the miR-1287-5p/DNA damage inducible transcript 4 (DDIT4) axis on the proliferation, apoptosis and invasion of ovarian cancer SKOV3 cells. Methods: Tissue samples of cancer and adjacent tissues from 27 patients with ovarian cancer who underwent surgery at Suizhou Hospital Affiliated to Hubei University of Medicine between June 2023 and June 2024 were collected. Normal human ovarian epithelial cells IOSE80 and ovarian cancer cells SKOV3, CAOV3 and A2780 were also collected. RT-qPCR was used to detect the expressions of lncRNA NEAT1, miR-1287-5p and DDIT4 mRNA in ovarian cancer tissues and cells. SKOV3 cells were divided into the Ctrl group, the si-NC group, the si-NEAT1 group, the si-NEAT1 + anti-miR-NC group, the si-NEAT1 + anti-miR-1287-5p group, the si-NEAT1 + vector group, and the si-NEAT1 + OE-DDIT4 group. The CCK-8 assay, colony formation assay, flow cytometry, and Transwell assay were used to detect the proliferation, apoptosis, and invasion abilities of cells in each group. The WB method was used to detect the protein levels of DDIT4, cyclin D1, p53, and migration-invasion enhancer 1 (MIEN1) in the cells. The dual-luciferase reporter gene was used to verify the targeted binding relationship between lncRNA NEAT1 and miR-1287-5p/DDIT4. The RNA pull-down experiment and RNA immunoprecipitation experiment were used respectively to verify the target binding relationships between lncRNA NEAT1 and miR-1287-5p, and between miR-1287-5p and DDIT4. Additionally, the pcDNA group (transfected with empty vector pcDNA3.1) and the pc-NEAT1 group (transfected with pcDNA-NEAT1) were established to validate the overexpression effects of NEAT1. Results: The expression levels of lncRNA NEAT1 and DDIT4 mRNA in ovarian cancer tissues were significantly higher than those in adjacent tissues (P < 0.05), while the expression level of miR-1287-5p was significantly lower than that in adjacent tissues (P < 0.05). After knockdown of lncRNA NEAT1, compared with those in the Ctrl group and the si-NC group, the expressions of lncRNA NEAT1 and DDIT4 mRNA, the number of colony formation, the cell proliferation activity, the number of cell invasion, and the expressions of DDIT4, cyclin D1, and MIEN1 proteins in the si-NEAT1 group all decreased significantly (all P < 0.05), while the expression of miR-1287-5p, the apoptosis rate, and the expression of p53 protein increased significantly (all P < 0.05). Conversely, overexpression of lncRNA NEAT1 decreased miR-1287-5p expression and increased DDIT4 expression, showing opposite regulatory effects to the knockdown experiment. Further experiments proved that anti-miR-1287-5p or OE-DDIT4 might weaken the inhibitory effect of si-NEAT1 on the proliferation and invasion of SKOV3 cells, as well as its promoting effect on cell apoptosis. lncRNA NEAT1 targetedly regulates miR-1287-5p/DDIT4. Conclusion: lncRNA NEAT1 enhances SKOV3 cell proliferation and invasion, and inhibits cell apoptosis by targeting regulating the miR-1287-5p/DDIT4 axis.
LONG Yuanfeng
,
YANG Yan
,
BIAN Yuhang
,
DENG Yubin
,
CHEN Qiaoling
,
YANG Hang
,
ZHANG Ruolan
,
ZHAO Quanmeng
,
YANG Mi
,
BIE Jun
,
SONG Guiqin
,
LIU Kang
2026, 33(4):408-417.
Abstract:
[Abstract] Objective: To investigate the molecular mechanism by which X-linked zinc finger protein (ZFX) influenced the progression of esophageal squamous cell carcinoma (ESCC) through Nectin-4 expression and its role in activating the PI3K/AKT signaling pathway. Methods: Thirty pairs of ESCC tissue and adjacent tissue specimens surgically resected at Nanchong Central Hospital between August 2022 and July 2023 were collected. Human esophageal epithelial cells (HET-1A) and ESCC cell lines (KYSE-30, KYSE-150, KYSE-410, KYSE-510, and TE-1) were used. Nectin-4 was selected based on transcriptome sequencing data from 6 paired ESCC specimens collected between 2018 and 2019. Expression levels of Nectin-4 in ESCC tissues and cells were detected using the TIMER 2.0 database, RT-qPCR, Western blotting (WB), and immunohistochemistry (IHC). Nectin-4 was knocked down in KYSE-410 and KYSE-510 cells using shRNA technology. The effects of Nectin-4 knockdown on cell proliferation, migration, and invasion abilities were detected via CCK-8 assay, colony formation assay, scratch healing assay, and Transwell assay. WB analysis was performed to examine changes in PI3K/AKT pathway-related proteins and EMT-related proteins following Nectin-4 knockdown. Bioinformatics prediction combined with dual luciferase reporter assay identified and validated ZFX as an upstream transcriptional regulator of Nectin-4. Results: Comprehensive analysis revealed significantly higher Nectin-4 expression in ESCC tissues and cell lines compared with that in adjacent non-cancerous tissues and HET-1A cells (all P < 0.01). Functional studies revealed that Nectin-4 knockdown significantly inhibited proliferation activity, colony formation capacity, migration, and invasion capabilities in KYSE-410 and KYSE-510 cells (all P < 0.01). Mechanistically, knocking down Nectin-4 upregulated E-cadherin expression, downregulated N-cadherin expression in cells (both P < 0.01), and inhibited the phosphorylation of PI3K/AKT pathway-related proteins (P < 0.01). Conclusion: ZFX promotes ESCC progression by upregulating Nectin-4 and activating the PI3K/AKT pathway, identifying potential therapeutic targets for ESCC treatment.
[Abstract] Objective: To investigate the molecular mechanism by which X-linked zinc finger protein (ZFX) influenced the progression of esophageal squamous cell carcinoma (ESCC) through Nectin-4 expression and its role in activating the PI3K/AKT signaling pathway. Methods: Thirty pairs of ESCC tissue and adjacent tissue specimens surgically resected at Nanchong Central Hospital between August 2022 and July 2023 were collected. Human esophageal epithelial cells (HET-1A) and ESCC cell lines (KYSE-30, KYSE-150, KYSE-410, KYSE-510, and TE-1) were used. Nectin-4 was selected based on transcriptome sequencing data from 6 paired ESCC specimens collected between 2018 and 2019. Expression levels of Nectin-4 in ESCC tissues and cells were detected using the TIMER 2.0 database, RT-qPCR, Western blotting (WB), and immunohistochemistry (IHC). Nectin-4 was knocked down in KYSE-410 and KYSE-510 cells using shRNA technology. The effects of Nectin-4 knockdown on cell proliferation, migration, and invasion abilities were detected via CCK-8 assay, colony formation assay, scratch healing assay, and Transwell assay. WB analysis was performed to examine changes in PI3K/AKT pathway-related proteins and EMT-related proteins following Nectin-4 knockdown. Bioinformatics prediction combined with dual luciferase reporter assay identified and validated ZFX as an upstream transcriptional regulator of Nectin-4. Results: Comprehensive analysis revealed significantly higher Nectin-4 expression in ESCC tissues and cell lines compared with that in adjacent non-cancerous tissues and HET-1A cells (all P < 0.01). Functional studies revealed that Nectin-4 knockdown significantly inhibited proliferation activity, colony formation capacity, migration, and invasion capabilities in KYSE-410 and KYSE-510 cells (all P < 0.01). Mechanistically, knocking down Nectin-4 upregulated E-cadherin expression, downregulated N-cadherin expression in cells (both P < 0.01), and inhibited the phosphorylation of PI3K/AKT pathway-related proteins (P < 0.01). Conclusion: ZFX promotes ESCC progression by upregulating Nectin-4 and activating the PI3K/AKT pathway, identifying potential therapeutic targets for ESCC treatment.
2026, 33(4):418-428.
Abstract:
[Abstract] Objective: To investigate the expression characteristics and clinical prognostic value of centromere protein M (CENPM) in glioma, and its regulatory mechanisms on malignant biological behaviors, providing potential targets for precision therapy in glioma. Methods: Based on the Chinese Glioma Genome Atlas (CGGA) and the Cancer Genome Atlas (TCGA) database, the expression of CENPM in glioma and its correlation with patients' clinicopathological features and prognosis were analyzed. Gene Ontology (GO) analysis, Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis, and single-cell transcriptome analysis were performed to explore the biological functions and mechanisms of CENPM. WB was used to detect CENPM expressions in glioma cell lines (LN-18, LN-229, U-138MG, U-251MG) and a normal glial cell line (HEB). After constructing CENPM knockdown cell lines, the alterations in malignant phenotypes were assessed using CCK-8, colony formation, Transwell, and wound healing assays. Results: CENPM was significantly upregulated in WHO high-grade gliomas (P < 0.05) and positively correlated with tumor malignancy. Patients in the high-expression group had significantly shorter overall survival than those in the low-expression group (P < 0.01), and Cox regression confirmed CENPM as an independent risk factor for glioma prognosis (P < 0.05). Functional enrichment analysis showed that CENPM-related genes were primarily enriched in cell cycle regulation, the PI3K-Akt pathway, and immune-related processes. Single-cell analysis indicated that CENPM was primarily highly expressed in CD8+ T cells and regulated cell communication through the PTN-PTPRZ1/NCL ligand-receptor pair. In vitro experiments confirmed that CENPM expression was higher in glioma cell lines than in normal glial cells (LN-18: P < 0.01, LN-229: P < 0.05); knockdown of CENPM significantly inhibited migration (P < 0.05) but enhanced colony formation, suggesting its dual regulatory role in tumor progression. Conclusion: As an independent prognostic risk factor for glioma, CENPM drives tumor progression by regulating the cell cycle, PTN pathway, and immune microenvironment. Its differential regulatory mechanism (inhibiting migration, promoting proliferation) has potential clinical translational value and can serve as a candidate marker for molecular typing and targeted therapy.
[Abstract] Objective: To investigate the expression characteristics and clinical prognostic value of centromere protein M (CENPM) in glioma, and its regulatory mechanisms on malignant biological behaviors, providing potential targets for precision therapy in glioma. Methods: Based on the Chinese Glioma Genome Atlas (CGGA) and the Cancer Genome Atlas (TCGA) database, the expression of CENPM in glioma and its correlation with patients' clinicopathological features and prognosis were analyzed. Gene Ontology (GO) analysis, Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis, and single-cell transcriptome analysis were performed to explore the biological functions and mechanisms of CENPM. WB was used to detect CENPM expressions in glioma cell lines (LN-18, LN-229, U-138MG, U-251MG) and a normal glial cell line (HEB). After constructing CENPM knockdown cell lines, the alterations in malignant phenotypes were assessed using CCK-8, colony formation, Transwell, and wound healing assays. Results: CENPM was significantly upregulated in WHO high-grade gliomas (P < 0.05) and positively correlated with tumor malignancy. Patients in the high-expression group had significantly shorter overall survival than those in the low-expression group (P < 0.01), and Cox regression confirmed CENPM as an independent risk factor for glioma prognosis (P < 0.05). Functional enrichment analysis showed that CENPM-related genes were primarily enriched in cell cycle regulation, the PI3K-Akt pathway, and immune-related processes. Single-cell analysis indicated that CENPM was primarily highly expressed in CD8+ T cells and regulated cell communication through the PTN-PTPRZ1/NCL ligand-receptor pair. In vitro experiments confirmed that CENPM expression was higher in glioma cell lines than in normal glial cells (LN-18: P < 0.01, LN-229: P < 0.05); knockdown of CENPM significantly inhibited migration (P < 0.05) but enhanced colony formation, suggesting its dual regulatory role in tumor progression. Conclusion: As an independent prognostic risk factor for glioma, CENPM drives tumor progression by regulating the cell cycle, PTN pathway, and immune microenvironment. Its differential regulatory mechanism (inhibiting migration, promoting proliferation) has potential clinical translational value and can serve as a candidate marker for molecular typing and targeted therapy.
2026, 33(4):429-438.
Abstract:
[Abstract] Objective: To comprehensively elucidate the potential mechanisms of gut microbiota in the occurrence and development of cholangiocarcinoma (CCA) and identify related key genes through integrative multi-omics analysis. Methods: Based on 16S rRNA sequencing data from the SRA database, the gut microbiota composition of CCA patients was compared with that of healthy controls. Mendelian randomization (MR) analysis was employed to assess the genetic association between specific microbiota and CCA risk. Relevant metabolites and genes were obtained from the gutMGene and GeneCards databases for metabolic and functional enrichment analyses. GEO single-cell transcriptomic data (GSE213452) was integrated to characterize the cellular composition of the tumor microenvironment, with a particular focus on T cell subsets and their functional states. The expression differences of key candidate genes were validated using the TCGA-CHOL dataset. Results: Compared with the healthy control group, the gut microbiota composition of CCA patients was significantly altered, characterized by an abnormal enrichment of the phylum Proteobacteria (LDA > 4). MR analysis further demonstrated that genetic predispositions to both the order Enterobacterales and the family Enterobacteriaceae were positively associated with the risk of CCA. Metabolic pathway enrichment analysis suggested that microbiota-related metabolites were mainly involved in pathways such as purine metabolism and glycolysis/gluconeogenesis; functional enrichment analysis showed that related genes were significantly enriched in inflammatory-immune pathways including NOD-like receptor, IL-17, Toll-like receptor, and NF-κB signaling pathways. Single-cell transcriptomic analysis revealed a significantly increased proportion of cancer cells (P < 0.05) and an elevated T cell proportion (from 20.7% to 39.2%) in CCA tissues. Pseudotime analysis indicated that MKI67+ T cells were at a late differentiation stage and exhibited high proliferative features. Differential genes of these T cells intersected with microbiota-related genes, among which SERPINA1 and IFNG showed significant changes in expression in the tumor immune microenvironment (P < 0.001) and may play a core regulatory role. Validation using the TCGA-CHOL dataset revealed that SERPINA1 was significantly downregulated in CCA tumor tissues (P < 0.001), whereas IFNG showed no significant difference between tumor and normal tissues (P > 0.05). Conclusion: Gut microbiota dysbiosis, particularly the abnormal proliferation of Enterobacteriaceae, may promote CCA progression via a metabolic-immune regulatory network. Specifically, alterations in T cell function are closely linked to the differentiated expression patterns of the key genes (SERPINA1 and IFNG) within MKI67+ T cells.
[Abstract] Objective: To comprehensively elucidate the potential mechanisms of gut microbiota in the occurrence and development of cholangiocarcinoma (CCA) and identify related key genes through integrative multi-omics analysis. Methods: Based on 16S rRNA sequencing data from the SRA database, the gut microbiota composition of CCA patients was compared with that of healthy controls. Mendelian randomization (MR) analysis was employed to assess the genetic association between specific microbiota and CCA risk. Relevant metabolites and genes were obtained from the gutMGene and GeneCards databases for metabolic and functional enrichment analyses. GEO single-cell transcriptomic data (GSE213452) was integrated to characterize the cellular composition of the tumor microenvironment, with a particular focus on T cell subsets and their functional states. The expression differences of key candidate genes were validated using the TCGA-CHOL dataset. Results: Compared with the healthy control group, the gut microbiota composition of CCA patients was significantly altered, characterized by an abnormal enrichment of the phylum Proteobacteria (LDA > 4). MR analysis further demonstrated that genetic predispositions to both the order Enterobacterales and the family Enterobacteriaceae were positively associated with the risk of CCA. Metabolic pathway enrichment analysis suggested that microbiota-related metabolites were mainly involved in pathways such as purine metabolism and glycolysis/gluconeogenesis; functional enrichment analysis showed that related genes were significantly enriched in inflammatory-immune pathways including NOD-like receptor, IL-17, Toll-like receptor, and NF-κB signaling pathways. Single-cell transcriptomic analysis revealed a significantly increased proportion of cancer cells (P < 0.05) and an elevated T cell proportion (from 20.7% to 39.2%) in CCA tissues. Pseudotime analysis indicated that MKI67+ T cells were at a late differentiation stage and exhibited high proliferative features. Differential genes of these T cells intersected with microbiota-related genes, among which SERPINA1 and IFNG showed significant changes in expression in the tumor immune microenvironment (P < 0.001) and may play a core regulatory role. Validation using the TCGA-CHOL dataset revealed that SERPINA1 was significantly downregulated in CCA tumor tissues (P < 0.001), whereas IFNG showed no significant difference between tumor and normal tissues (P > 0.05). Conclusion: Gut microbiota dysbiosis, particularly the abnormal proliferation of Enterobacteriaceae, may promote CCA progression via a metabolic-immune regulatory network. Specifically, alterations in T cell function are closely linked to the differentiated expression patterns of the key genes (SERPINA1 and IFNG) within MKI67+ T cells.
2026, 33(4):439-445.
Abstract:
[Abstract] TLC domain containing 1 (TLCD1) is a key rate-limiting enzyme catalyzing the synthesis of phosphatidylethanolamine (PE) from lysophosphatidylethanolamine (LPE), playing a central regulatory role in tumor lipid metabolism reprogramming. TLCD1 is highly expressed in various malignant tumors, affecting tumor proliferation and metastasis through regulating PE synthesis, and is closely associated with poor prognosis. Furthermore, it can reshape the tumor immune microenvironment and promote immune evasion. This review systematically summarizes the molecular mechanisms of TLCD1 in lipid metabolism regulation and immune modulation, explores its potential as a therapeutic target for anti-tumor therapy and as a biomarker for immunotherapy response, providing new insights for optimizing precision tumor treatment strategies.
[Abstract] TLC domain containing 1 (TLCD1) is a key rate-limiting enzyme catalyzing the synthesis of phosphatidylethanolamine (PE) from lysophosphatidylethanolamine (LPE), playing a central regulatory role in tumor lipid metabolism reprogramming. TLCD1 is highly expressed in various malignant tumors, affecting tumor proliferation and metastasis through regulating PE synthesis, and is closely associated with poor prognosis. Furthermore, it can reshape the tumor immune microenvironment and promote immune evasion. This review systematically summarizes the molecular mechanisms of TLCD1 in lipid metabolism regulation and immune modulation, explores its potential as a therapeutic target for anti-tumor therapy and as a biomarker for immunotherapy response, providing new insights for optimizing precision tumor treatment strategies.
2026, 33(4):446-453.
Abstract:
[Abstract] Obesity is a risk factor for various malignant tumors and is often associated with poor prognosis. However, in certain tumors such as melanoma (MM) and non-small cell lung cancer (NSCLC), obese patients exhibit better survival benefits from immunotherapy than normal-weight patients, a phenomenon known as the "obesity paradox," whose underlying mechanisms may be closely related to obesity-associated immune dysregulation. Recent studies have shown that obesity not only induces systemic immune dysregulation through adipokine imbalance and chronic inflammation but also directly impairs the functions of CD8+ T cells, natural killer (NK) cells, and dendritic cells (DCs) in the tumor microenvironment (TME) through metabolic reprogramming (e.g., lipid overload, enhanced fatty acid oxidation), while driving tumor-associated macrophages (TAMs) to highly express PD-1, forming a unique immunosuppressive microenvironment. However, due to limitations of preclinical models, confounding factors in clinical data, and the singularity of traditional obesity definition indicators (such as BMI), elucidating the mechanisms of the "obesity paradox" and its clinical translation faces many challenges. Therefore, this review combs the dual effects of obesity in tumor immunotherapy, focuses on elucidating its remodeling mechanisms of the TME metabolic-immune regulatory network, explores multidimensional assessment strategies beyond BMI and the application prospects of better preclinical models, aiming to provide new ideas for precision immunotherapy in obese cancer patients.
[Abstract] Obesity is a risk factor for various malignant tumors and is often associated with poor prognosis. However, in certain tumors such as melanoma (MM) and non-small cell lung cancer (NSCLC), obese patients exhibit better survival benefits from immunotherapy than normal-weight patients, a phenomenon known as the "obesity paradox," whose underlying mechanisms may be closely related to obesity-associated immune dysregulation. Recent studies have shown that obesity not only induces systemic immune dysregulation through adipokine imbalance and chronic inflammation but also directly impairs the functions of CD8+ T cells, natural killer (NK) cells, and dendritic cells (DCs) in the tumor microenvironment (TME) through metabolic reprogramming (e.g., lipid overload, enhanced fatty acid oxidation), while driving tumor-associated macrophages (TAMs) to highly express PD-1, forming a unique immunosuppressive microenvironment. However, due to limitations of preclinical models, confounding factors in clinical data, and the singularity of traditional obesity definition indicators (such as BMI), elucidating the mechanisms of the "obesity paradox" and its clinical translation faces many challenges. Therefore, this review combs the dual effects of obesity in tumor immunotherapy, focuses on elucidating its remodeling mechanisms of the TME metabolic-immune regulatory network, explores multidimensional assessment strategies beyond BMI and the application prospects of better preclinical models, aiming to provide new ideas for precision immunotherapy in obese cancer patients.
2026, 33(4):454-459.
Abstract:
[Abstract] Myelodysplastic syndromes (MDS) are a group of myeloid malignancies originating from hematopoietic stem cells, with an increasing incidence rate year by year. In recent years, chimeric antigen receptor gene-modified T lymphocyte (CAR-T cell) therapy targeting specific antigens has achieved remarkable success in the field of hematological tumors, opening up new directions for the treatment of MDS. The key to promoting the successful application of CAR-T cell therapy lies in finding MDS-specific target antigens. Studies have found that CD44 splice variant CD44v6 is generally highly expressed in early-stage ineffective erythropoiesis in MDS patients, suggesting it is a highly promising therapeutic target. This review systematically summarizes the new research progress on CD44v6 regulating the pathological process of MDS, focuses on analyzing the clinical translational value of innovative therapeutic strategies targeting CD44v6 (including CAR-T cell therapy), and explores its application prospects in promoting precision personalized treatment of MDS.
[Abstract] Myelodysplastic syndromes (MDS) are a group of myeloid malignancies originating from hematopoietic stem cells, with an increasing incidence rate year by year. In recent years, chimeric antigen receptor gene-modified T lymphocyte (CAR-T cell) therapy targeting specific antigens has achieved remarkable success in the field of hematological tumors, opening up new directions for the treatment of MDS. The key to promoting the successful application of CAR-T cell therapy lies in finding MDS-specific target antigens. Studies have found that CD44 splice variant CD44v6 is generally highly expressed in early-stage ineffective erythropoiesis in MDS patients, suggesting it is a highly promising therapeutic target. This review systematically summarizes the new research progress on CD44v6 regulating the pathological process of MDS, focuses on analyzing the clinical translational value of innovative therapeutic strategies targeting CD44v6 (including CAR-T cell therapy), and explores its application prospects in promoting precision personalized treatment of MDS.
2026, 33(4):460-467.
Abstract:
[Abstract] Therapeutic human papillomavirus (HPV) vaccines induce specific immune responses against viral oncoproteins to achieve the goals of eliminating persistent viral infection and inhibiting tumor progression. Various therapeutic vaccines based on different platforms have shown good safety and certain immunogenicity in clinical studies, but clinical efficacy remains limited by factors such as delivery efficiency, insufficient immunogenicity, and immune evasion. This review focuses on the key technological approaches of therapeutic HPV vaccines, systematically summarizes the mechanisms and representative clinical evidence of various platforms, highlights the latest progress in novel nucleic acid platforms and delivery technologies, exploration of new targets such as E2/E5, heterologous prime-boost immunization, and combination therapeutic strategies, and summarizes current evidence gaps and translational challenges, providing a basis for subsequent vaccine regimen optimization, combination therapeutic strategy design, and clinical translation.
[Abstract] Therapeutic human papillomavirus (HPV) vaccines induce specific immune responses against viral oncoproteins to achieve the goals of eliminating persistent viral infection and inhibiting tumor progression. Various therapeutic vaccines based on different platforms have shown good safety and certain immunogenicity in clinical studies, but clinical efficacy remains limited by factors such as delivery efficiency, insufficient immunogenicity, and immune evasion. This review focuses on the key technological approaches of therapeutic HPV vaccines, systematically summarizes the mechanisms and representative clinical evidence of various platforms, highlights the latest progress in novel nucleic acid platforms and delivery technologies, exploration of new targets such as E2/E5, heterologous prime-boost immunization, and combination therapeutic strategies, and summarizes current evidence gaps and translational challenges, providing a basis for subsequent vaccine regimen optimization, combination therapeutic strategy design, and clinical translation.
2026, 33(4):468-473.
Abstract:
[Abstract] Nanocarriers are prone to rapid clearance by the mononuclear phagocyte system (MPS) in tumor-targeted therapy, leading to reduced drug bioavailability and limited anti-tumor efficacy. The CD47 peptide-mediated "stealth" strategy, by mimicking the "don't eat me" signal, can effectively inhibit macrophage phagocytosis of nanocarriers, serving as an effective means to prolong the in vivo circulation half-life of drugs and enhance tumor-targeted delivery efficiency. This review summarizes the mechanism of action, carrier types, major application progress, key challenges, and potential solutions of the CD47 peptide "stealth" strategy. It focuses on the structure-activity relationship of CD47 peptide modification, the applicability differences of different nanocarrier platforms, research gaps in long-term delivery efficiency and in vivo stability, as well as the construction of standardized evaluation systems and future development directions. The goal is to promote CD47 peptide-modified nanocarriers as an important stealth-capable platform for precision tumor delivery, providing new strategies for improving the in vivo delivery efficiency and anti-tumor efficacy of nanomedicines.
[Abstract] Nanocarriers are prone to rapid clearance by the mononuclear phagocyte system (MPS) in tumor-targeted therapy, leading to reduced drug bioavailability and limited anti-tumor efficacy. The CD47 peptide-mediated "stealth" strategy, by mimicking the "don't eat me" signal, can effectively inhibit macrophage phagocytosis of nanocarriers, serving as an effective means to prolong the in vivo circulation half-life of drugs and enhance tumor-targeted delivery efficiency. This review summarizes the mechanism of action, carrier types, major application progress, key challenges, and potential solutions of the CD47 peptide "stealth" strategy. It focuses on the structure-activity relationship of CD47 peptide modification, the applicability differences of different nanocarrier platforms, research gaps in long-term delivery efficiency and in vivo stability, as well as the construction of standardized evaluation systems and future development directions. The goal is to promote CD47 peptide-modified nanocarriers as an important stealth-capable platform for precision tumor delivery, providing new strategies for improving the in vivo delivery efficiency and anti-tumor efficacy of nanomedicines.
2026, 33(4):474-476.
Abstract:
[Abstract] Uterine leiomyoma is a common benign tumor in women, but distant metastasis is extremely rare in clinical practice. This article retrospectively analyzes the clinical data of 6 patients with uterine leiomyoma metastasis at different sites who were treated at Nanjing Drum Tower Hospital Affiliated to Nanjing University Medical School from January 2019 to August 2023, summarizing their clinical characteristics, diagnosis and treatment plans, pathological features, and prognosis. Meanwhile, combined with literature review, it explores the pathogenesis and clinical diagnosis and treatment strategies of metastasizing uterine leiomyoma, aiming to improve clinical recognition of this disease and provide reference for its diagnosis and treatment.
[Abstract] Uterine leiomyoma is a common benign tumor in women, but distant metastasis is extremely rare in clinical practice. This article retrospectively analyzes the clinical data of 6 patients with uterine leiomyoma metastasis at different sites who were treated at Nanjing Drum Tower Hospital Affiliated to Nanjing University Medical School from January 2019 to August 2023, summarizing their clinical characteristics, diagnosis and treatment plans, pathological features, and prognosis. Meanwhile, combined with literature review, it explores the pathogenesis and clinical diagnosis and treatment strategies of metastasizing uterine leiomyoma, aiming to improve clinical recognition of this disease and provide reference for its diagnosis and treatment.
联系方式
- 《中国肿瘤生物治疗杂志》
- 1994年创刊
- 主办单位：Chinese Society of Immunology, Chinese Anti-cancer Association
- 邮编：200433
- 电话：021-81871002-22
- 电子邮箱：cjcb@biother.cn
- 网址:http://www.biother.cn
- 刊号：ISSN 1007-385X
- CN 31-1725/R
- 国内定价： ￥20元/册
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Chinese Journal Of Cancer Biotheray ® 2026 All Rights Reserved
Supported by:Beijing E-Tiller Technology Development Co., Ltd.
Chinese Journal Of Cancer Biotheray ® 2026 All Rights Reserved
Supported by:Beijing E-Tiller Technology Development Co., Ltd.