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2025,32(4):347-355, DOI: 10.3872/j.issn.1007-385X.2025.04.001
Abstract:
[Abstract] Alternative splicing, a post-transcriptional regulatory mechanism of gene expression, contributes to the diversity of the transcriptome and proteome in eukaryotes. However, aberrant alternative splicing serves as a significant driver of tumor progression, where abnormal splicing in tumor cells, immune cells, and other cell types within the tumor microenvironment collectively results in malignant behaviors of cancer cells, immune evasion, and the immunosuppressive milieu that supports tumor advancement. Targeting tumor-associated spliceosomes, splicing regulatory factors, splicing isoforms and variants, as well as tumor neoantigens generated by aberrant alternative splicing, has emerged as a novel strategy in cancer biotherapy. Some alternative splicing-based antitumor biotherapy programs have progressed to phase Ⅰ clinical trials. Alternative splicing-based tumor therapy still faces scientific and technological challenges such as safety, optimization of long-read sequencing and bioinformatics algorithm, and nucleic acid drug delivery. Addressing these challenges will provide new tumor therapy strategies and open up new frontiers for precisely screening tumor-related targets and highly immunogenic neoantigens, overcoming drug resistance in traditional therapies, and enhancing the efficacy of immune checkpoint blockade, CAR-T cell therapy, and other treatments.
[Abstract] Alternative splicing, a post-transcriptional regulatory mechanism of gene expression, contributes to the diversity of the transcriptome and proteome in eukaryotes. However, aberrant alternative splicing serves as a significant driver of tumor progression, where abnormal splicing in tumor cells, immune cells, and other cell types within the tumor microenvironment collectively results in malignant behaviors of cancer cells, immune evasion, and the immunosuppressive milieu that supports tumor advancement. Targeting tumor-associated spliceosomes, splicing regulatory factors, splicing isoforms and variants, as well as tumor neoantigens generated by aberrant alternative splicing, has emerged as a novel strategy in cancer biotherapy. Some alternative splicing-based antitumor biotherapy programs have progressed to phase Ⅰ clinical trials. Alternative splicing-based tumor therapy still faces scientific and technological challenges such as safety, optimization of long-read sequencing and bioinformatics algorithm, and nucleic acid drug delivery. Addressing these challenges will provide new tumor therapy strategies and open up new frontiers for precisely screening tumor-related targets and highly immunogenic neoantigens, overcoming drug resistance in traditional therapies, and enhancing the efficacy of immune checkpoint blockade, CAR-T cell therapy, and other treatments.
2025,32(4):356-363, DOI: 10.3872/j.issn.1007-385X.2025.04.002
Abstract:
[Abstract] Objective: To investigate the impact of locally IL-2-secreting CAR-T cells (Syn.CD19.IL-2 CAR-T cells) constructed using a novel single-vector SynNotch system on the function of conventional CD19 CAR-T cells. Methods: Building upon our previously established single-vector SynNotch system, the CD19-specific FMC63 antibody was integrated with an IL-2 expression module to prepare Syn.CD19.IL-2 CAR-T cells through T cell transduction using a self-inactivating retroviral vector. For validation experiments, cells were divided into the Syn.CD19.IL-2 CAR-T cell group and the untransduced T cells group. ELISA was used to detect IL-2 secretion levels after antigen stimulation. The CFSE staining assay was implemented to evaluate the effects of IL-2 secretion on the proliferation of CD19 CAR-T cells when CD19 CAR-T cells were co-cultured with Raji-Luc or SW620-CD19-Luc cells in the presence of Syn. CD19. IL-2 CAR-T cells. Flow cytometry was employed to detect CD69 expression and monitor the activation status of CD19 CAR-T cells when co-cultured with Raji-Luc cells in the condition of Syn.CD19.IL-2 CAR-T cells secreting IL-2. Results: The self-inactivating retroviral vector Syn.CD19.IL-2 CAR were successfully constructed and Syn.CD19.IL-2 CAR-T cells with a viral titer >1 × 10? copies/mL and transduction efficiency of 37.1% were generated. After antigen stimulation, SynNotch CAR-T cells demonstrated significantly elevated IL-2 secretion compared with the untransduced T cell group (P < 0.001). When Syn. CD19.IL-2 CAR-T cells secreted IL-2, the CD19 CAR-T cells exhibited enhanced proliferative capacity and elevated activation level (all P < 0.001). Conclusion: Successfully constructed Syn.CD19.IL-2 CAR-T cells can significantly enhance the proliferative capacity and activation ability of conventional CD19 CAR-T cells.
[Abstract] Objective: To investigate the impact of locally IL-2-secreting CAR-T cells (Syn.CD19.IL-2 CAR-T cells) constructed using a novel single-vector SynNotch system on the function of conventional CD19 CAR-T cells. Methods: Building upon our previously established single-vector SynNotch system, the CD19-specific FMC63 antibody was integrated with an IL-2 expression module to prepare Syn.CD19.IL-2 CAR-T cells through T cell transduction using a self-inactivating retroviral vector. For validation experiments, cells were divided into the Syn.CD19.IL-2 CAR-T cell group and the untransduced T cells group. ELISA was used to detect IL-2 secretion levels after antigen stimulation. The CFSE staining assay was implemented to evaluate the effects of IL-2 secretion on the proliferation of CD19 CAR-T cells when CD19 CAR-T cells were co-cultured with Raji-Luc or SW620-CD19-Luc cells in the presence of Syn. CD19. IL-2 CAR-T cells. Flow cytometry was employed to detect CD69 expression and monitor the activation status of CD19 CAR-T cells when co-cultured with Raji-Luc cells in the condition of Syn.CD19.IL-2 CAR-T cells secreting IL-2. Results: The self-inactivating retroviral vector Syn.CD19.IL-2 CAR were successfully constructed and Syn.CD19.IL-2 CAR-T cells with a viral titer >1 × 10? copies/mL and transduction efficiency of 37.1% were generated. After antigen stimulation, SynNotch CAR-T cells demonstrated significantly elevated IL-2 secretion compared with the untransduced T cell group (P < 0.001). When Syn. CD19.IL-2 CAR-T cells secreted IL-2, the CD19 CAR-T cells exhibited enhanced proliferative capacity and elevated activation level (all P < 0.001). Conclusion: Successfully constructed Syn.CD19.IL-2 CAR-T cells can significantly enhance the proliferative capacity and activation ability of conventional CD19 CAR-T cells.
2025,32(4):364-370, DOI: 10.3872/j.issn.1007-385X.2025.04.003
Abstract:
[Abstract] Objective: To investigate the expression of homeobox protein C4 (HOXC4) in gastric cancer tissues and cells, as well as its effects on the proliferation, migration and invasion of gastric cancer cells and the underlying mechanisms. Methods: The cancer and adjacent tissue specimens surgically removed from 16 patients with advanced gastric cancer at the Department of Oncology, Nanyang First People’s Hospital, between May 2020 and April 2021 were collected. Additionally, human normal gastric epithelial cells (GES-1) and gastric cancer cell lines (AGS, SGC-790, and MGC-803) were included. Western blot (WB) was performed to detect HOXC4 expression in gastric cancer tissues and cells. RNA interference technology was used to knockdown or overexpress HOXC4 in SGC-790 and AGS cells, with experimental groups divided as follows: the sh-HOXC4#1 group, sh-HOXC4#2 group, sh-Con group, sh-HOXC4 + pc-integrin β1 group, pc-HOXC4 group, pc-Con group, and pc-HOXC4 + pc-integrin β1 group. EdU assay, CCK-8 assay, and Transwell assay were employed to evaluate the effects of HOXC4 knockdown or overexpression on cell viability, proliferation, migration,invasion, and integrin β1 expression in each group. A tumor-bearing mouse model was established using HOXC4-knockdown AGS cells to observe the impact of HOXC4 knockdown on tumor volume and the expressions of Ki67 and integrin β1 proteins in xenograft tissues. Results: The expression of HOXC4 in gastric cancer tissues and cells was significantly up-regulated (all P < 0.01). Compared with those in the sh-Con group, the expression levels of HOXC4 and integrin β1 in SGC-790 and AGS cells, and the cell viability, proliferation, migration and invasion ability decreased significantly in sh-HOXC4#1 and sh-HOXC4#2 groups (all P < 0.01).Compared with those in the sh-HOXC4 group, the cell viability, invasion and migration abilities of cells in the sh-HOXC4 + pc-integrin β1 group increased significantly (all P < 0.01). Compared with those in the pc-Con group, the cell viability, invasion and migration abilities of cells in the pc-HOXC4 group increased significantly (all P < 0.01). Compared with those in the pc-HOXC4 group, the cell viability, invasion and migration abilities of cells in the pc-HOXC4+integrin β1-shRNA group decreased significantly (all P < 0.01). Compared with those in the sh-Con group, the tumor grew slowly, and the volume decreased, and the expressions of Ki67 and integrin β1 decreased significantly in the sh-HOXC4#1 and sh-HOXC4#2 groups (all P < 0.01). Conclusion: The expression of HOXC4 is up-regulated in gastric cancer tissues and cells, and it promotes the proliferation, migration and invasion of gastric cancer cells by activating the integrin β1 signaling pathway.
[Abstract] Objective: To investigate the expression of homeobox protein C4 (HOXC4) in gastric cancer tissues and cells, as well as its effects on the proliferation, migration and invasion of gastric cancer cells and the underlying mechanisms. Methods: The cancer and adjacent tissue specimens surgically removed from 16 patients with advanced gastric cancer at the Department of Oncology, Nanyang First People’s Hospital, between May 2020 and April 2021 were collected. Additionally, human normal gastric epithelial cells (GES-1) and gastric cancer cell lines (AGS, SGC-790, and MGC-803) were included. Western blot (WB) was performed to detect HOXC4 expression in gastric cancer tissues and cells. RNA interference technology was used to knockdown or overexpress HOXC4 in SGC-790 and AGS cells, with experimental groups divided as follows: the sh-HOXC4#1 group, sh-HOXC4#2 group, sh-Con group, sh-HOXC4 + pc-integrin β1 group, pc-HOXC4 group, pc-Con group, and pc-HOXC4 + pc-integrin β1 group. EdU assay, CCK-8 assay, and Transwell assay were employed to evaluate the effects of HOXC4 knockdown or overexpression on cell viability, proliferation, migration,invasion, and integrin β1 expression in each group. A tumor-bearing mouse model was established using HOXC4-knockdown AGS cells to observe the impact of HOXC4 knockdown on tumor volume and the expressions of Ki67 and integrin β1 proteins in xenograft tissues. Results: The expression of HOXC4 in gastric cancer tissues and cells was significantly up-regulated (all P < 0.01). Compared with those in the sh-Con group, the expression levels of HOXC4 and integrin β1 in SGC-790 and AGS cells, and the cell viability, proliferation, migration and invasion ability decreased significantly in sh-HOXC4#1 and sh-HOXC4#2 groups (all P < 0.01).Compared with those in the sh-HOXC4 group, the cell viability, invasion and migration abilities of cells in the sh-HOXC4 + pc-integrin β1 group increased significantly (all P < 0.01). Compared with those in the pc-Con group, the cell viability, invasion and migration abilities of cells in the pc-HOXC4 group increased significantly (all P < 0.01). Compared with those in the pc-HOXC4 group, the cell viability, invasion and migration abilities of cells in the pc-HOXC4+integrin β1-shRNA group decreased significantly (all P < 0.01). Compared with those in the sh-Con group, the tumor grew slowly, and the volume decreased, and the expressions of Ki67 and integrin β1 decreased significantly in the sh-HOXC4#1 and sh-HOXC4#2 groups (all P < 0.01). Conclusion: The expression of HOXC4 is up-regulated in gastric cancer tissues and cells, and it promotes the proliferation, migration and invasion of gastric cancer cells by activating the integrin β1 signaling pathway.
2025,32(4):371-377, DOI: 10.3872/j.issn.1007-385X.2025.04.004
Abstract:
[Abstract] Objective: To investigate the expression of potassium calcium-activated channel subfamily N member 4 (KCNN4) in pancreatic cancer tissues and its impact on tumor progression, and to explore its role in clinical diagnosis and prognosis evaluation of pancreatic cancer. Methods: Using the GEPIA2 data analysis platform, the expression of KCNN4 in pancreatic cancer tissues and its correlation with patient prognosis were analyzed by integrating data from the TCGA and GTEx databases. Cancerous and adjacent non cancerous tissues from 24 patients with pancreatic cancer who underwent surgical resection at ChangHai Hospital of the Naval Medical University were collected. The expression of KCNN4 in pancreatic cancer tissues was validated using qPCR, Western blotting, and immunohistochemical staining. The expression of KCNN4 in human pancreatic cancer cell lines BXPC3 and PANC-1 was knocked down using shRNA. CCK-8 and colony formation assays were performed to detect tumor cell proliferation and growth. A murine KPC cell pancreatic cancer model was established to investigate the effects of KCNN4 knockdown on the growth of orthotopic pancreatic tumor and overall survival (OS) in mice. Results: Analysis of TCGA and GTEx data revealed that KCNN4 was highly expressed in pancreatic cancer tissues (P < 0.05) and was associated with shortened OS and disease-free survival (DFS) in patients (both P < 0.05). The expression levels of KCNN4 mRNA and protein were significantly elevated in pancreatic cancer tissues compared with those in adjacent non-cancerous tissues (all P < 0.01). Knockdown of KCNN4 led to significantly reduced growth rates and fewer colony formations in pancreatic cancer cells (both P < 0.01). The murine orthotopic pancreatic tumor experiment revealed that KCNN4 knockdown inhibited tumor progression and prolonged the OS of mice. Conclusion: KCNN4, highly expressed in pancreatic cancer tissues, promotes pancreatic cancer cell proliferation and tumor progression, and its expression is closely associated with patient prognosis, suggesting that KCNN4 may serve as a promising target for clinical diagnosis and prognosis evaluation of pancreatic cancer.
[Abstract] Objective: To investigate the expression of potassium calcium-activated channel subfamily N member 4 (KCNN4) in pancreatic cancer tissues and its impact on tumor progression, and to explore its role in clinical diagnosis and prognosis evaluation of pancreatic cancer. Methods: Using the GEPIA2 data analysis platform, the expression of KCNN4 in pancreatic cancer tissues and its correlation with patient prognosis were analyzed by integrating data from the TCGA and GTEx databases. Cancerous and adjacent non cancerous tissues from 24 patients with pancreatic cancer who underwent surgical resection at ChangHai Hospital of the Naval Medical University were collected. The expression of KCNN4 in pancreatic cancer tissues was validated using qPCR, Western blotting, and immunohistochemical staining. The expression of KCNN4 in human pancreatic cancer cell lines BXPC3 and PANC-1 was knocked down using shRNA. CCK-8 and colony formation assays were performed to detect tumor cell proliferation and growth. A murine KPC cell pancreatic cancer model was established to investigate the effects of KCNN4 knockdown on the growth of orthotopic pancreatic tumor and overall survival (OS) in mice. Results: Analysis of TCGA and GTEx data revealed that KCNN4 was highly expressed in pancreatic cancer tissues (P < 0.05) and was associated with shortened OS and disease-free survival (DFS) in patients (both P < 0.05). The expression levels of KCNN4 mRNA and protein were significantly elevated in pancreatic cancer tissues compared with those in adjacent non-cancerous tissues (all P < 0.01). Knockdown of KCNN4 led to significantly reduced growth rates and fewer colony formations in pancreatic cancer cells (both P < 0.01). The murine orthotopic pancreatic tumor experiment revealed that KCNN4 knockdown inhibited tumor progression and prolonged the OS of mice. Conclusion: KCNN4, highly expressed in pancreatic cancer tissues, promotes pancreatic cancer cell proliferation and tumor progression, and its expression is closely associated with patient prognosis, suggesting that KCNN4 may serve as a promising target for clinical diagnosis and prognosis evaluation of pancreatic cancer.
2025,32(4):378-385, DOI: 10.3872/j.issn.1007-385X.2025.04.005
Abstract:
[Abstract] Objective: To investigate the effect of circular RNA (cireRNA) pumilio RNA binding family member 1 (PUM1) on the proliferation, migration, invasion and apoptosis of endometrial cancer (EC) Ishikawa cells by regulating the miR-337-3p/ nucleophosmin 1 (NPM1) axis. Methods: Ishikawa cells were selected and plasmid sh-circPUM1 and its negative control (sh-NC), anti-miR-337-3p and its negative control (anti-NC) were transfected into Ishikawa cells by RNA interference. The experiment cells were divided into the control group (non-transfected cells), sh-NC group, sh-circPUM1 group, sh-circPUM1 + anti-NC group and sh-circPUM1 + anti-miR-337-3p group. The qPCR method was applied to detect the expressions of circPUM1, miR-337-3p, and NPM1 mRNA in Ishikawa cells in each group. CCK-8 method, EdU staining method, Transwell assay, and flow cytometry were applied respectively to detect the effects of knocking down circPUM1 on the proliferation, migration, invasion and apoptosis of Ishikawa cells. Western blot was applied to detect the changes in the expressions of PCNA, NPM1, MMP-9, SNAIL, E-cadherin, BAX and C-caspase-3 proteins in Ishikawa cells. Dual luciferase reporter gene experiment was applied to verify the targeting relationship between circPUM1 and miR-337-3p, and between miR-337-3p and NPM1. Results: Cell proliferation ability, EdU positive cell rate, migration and invasion numbers, circPUM1, NPM1 mRNA and protein, the expressions of PCNA, NPM1, MMP-9 and SNAIL protein in Ishikawa cells in the sh-circPUM1 group were significantly lower than those in the sh-NC group and Control group (all P < 0.05); the apoptosis rate, the expressions of miR-337-3p, E-cadherin, BAX, and C-caspase-3 proteins were significantly higher than those in the sh-NC group and the Control group (all P < 0.05). Compared with those in the sh-circPUM1 group and the sh-circPUM1 + anti-NC group, the apoptosis rate, miR-337-3p, the expressions of E-cadherin, BAX, and C-caspase-3 proteins in the sh-circPUM1 + anti-miR 337-3p group were significantly lower (all P < 0.05); Cell proliferation ability, EdU positive cell rate, migration and invasion numbers, NPM1 mRNA and protein, the expressions of PCNA, NPM1, MMP-9, and SNAIL proteins were significantly higher (all P < 0.05). CircPUM1 might target and negatively regulate miR-337-3p, and miR-337-3p might target and negatively regulate NPM1. Conclusion: Knocking down circPUM1 can inhibit the malignant biological behavior of Ishikawa cells, which might be achieved by targeting the miR-337-3p/NPM1 axis.
[Abstract] Objective: To investigate the effect of circular RNA (cireRNA) pumilio RNA binding family member 1 (PUM1) on the proliferation, migration, invasion and apoptosis of endometrial cancer (EC) Ishikawa cells by regulating the miR-337-3p/ nucleophosmin 1 (NPM1) axis. Methods: Ishikawa cells were selected and plasmid sh-circPUM1 and its negative control (sh-NC), anti-miR-337-3p and its negative control (anti-NC) were transfected into Ishikawa cells by RNA interference. The experiment cells were divided into the control group (non-transfected cells), sh-NC group, sh-circPUM1 group, sh-circPUM1 + anti-NC group and sh-circPUM1 + anti-miR-337-3p group. The qPCR method was applied to detect the expressions of circPUM1, miR-337-3p, and NPM1 mRNA in Ishikawa cells in each group. CCK-8 method, EdU staining method, Transwell assay, and flow cytometry were applied respectively to detect the effects of knocking down circPUM1 on the proliferation, migration, invasion and apoptosis of Ishikawa cells. Western blot was applied to detect the changes in the expressions of PCNA, NPM1, MMP-9, SNAIL, E-cadherin, BAX and C-caspase-3 proteins in Ishikawa cells. Dual luciferase reporter gene experiment was applied to verify the targeting relationship between circPUM1 and miR-337-3p, and between miR-337-3p and NPM1. Results: Cell proliferation ability, EdU positive cell rate, migration and invasion numbers, circPUM1, NPM1 mRNA and protein, the expressions of PCNA, NPM1, MMP-9 and SNAIL protein in Ishikawa cells in the sh-circPUM1 group were significantly lower than those in the sh-NC group and Control group (all P < 0.05); the apoptosis rate, the expressions of miR-337-3p, E-cadherin, BAX, and C-caspase-3 proteins were significantly higher than those in the sh-NC group and the Control group (all P < 0.05). Compared with those in the sh-circPUM1 group and the sh-circPUM1 + anti-NC group, the apoptosis rate, miR-337-3p, the expressions of E-cadherin, BAX, and C-caspase-3 proteins in the sh-circPUM1 + anti-miR 337-3p group were significantly lower (all P < 0.05); Cell proliferation ability, EdU positive cell rate, migration and invasion numbers, NPM1 mRNA and protein, the expressions of PCNA, NPM1, MMP-9, and SNAIL proteins were significantly higher (all P < 0.05). CircPUM1 might target and negatively regulate miR-337-3p, and miR-337-3p might target and negatively regulate NPM1. Conclusion: Knocking down circPUM1 can inhibit the malignant biological behavior of Ishikawa cells, which might be achieved by targeting the miR-337-3p/NPM1 axis.
2025,32(4):386-391, DOI: 10.3872/j.issn.1007-385X.2025.04.006
Abstract:
[Abstract] Objective: To investigate the expression of circular RNA hsa_circ_0046701 in glioma tissues and its effect on the proliferation, migration and invasion of glioma U251 cells. Methods: Tumor tissue specimens and clinical data of fifty-two glioma patients treated surgically in Putuo People's Hospital Affiliated to Tongji University between June 2022 and March 2023 were collected, and another 30 normal brain tissue specimens were collected as controls. The expression level of hsa_circ_0046701 in glioma tissues was detected by qPCR to analyze the relationship between the level and clinical characteristics of the patient. Kaplan-Meier method was used to analyze the relationship between hsa_circ_0046701 level and survival prognosis. Using RNA interference technology, circ_0046701 overexpression and empty vector, siRNA-circ_0046701 and negative control (si-NC) plasmid were transfected into glioma U251 cells, respectively. The experiment cells were divided into the circ 0046701 OE group, Vector group, si-circ_0046701 group and si-NC group. CCK-8 method and Transwell assay were applied to detect the proliferation, migration and invasion abilities of cells in each group. Western blotting was applied to detect the expressions of vimentin, Snail, E-cadherin and cyclin D1 proteins in cells of each group. Results: The expression level of hsa_circ_0046701 in glioma tissues was significantly higher than that in normal brain tissues (P < 0.01). The percentage of patients with WHO glioma grading (grades Ⅲ~Ⅳ) in the hsa_circ_0046701 high-expression group was significantly higher than that of the hsa_circ_0046701 low expression group (P < 0.01). The OS of patients in the high expression group was significantly shorter than that of the low-expression group. Compared with those in the si-NC group, the proliferation ability of U251 cells in the si-circ_0046701 group was significantly reduced (P < 0.05 or P < 0.01), and the numbers of migrated and invaded cells decreased significantly (both P < 0.01). The expressions of vimentin, Snail, and cyclin D1 proteins in the cells was significantly reduced (all P < 0.01), while the expression of E-cadherin protein increased significantly (P < 0.01). Compared with those in the Vector group, the proliferation ability of U251cells in the circ_0046701 OE group increased significantly (P < 0.01); the numbers of migrated and invaded cells increased significantly (both P < 0.01); the expressions of vimentin, Snail, and cyclin D1 proteins in the cells increaseds significantly (all P < 0.01), and the expression of E-cadherin protein decreased significantly (P < 0.01). Conclusion: Circular RNA hsa_circ_0046701 is highly expressed in glioma tissues, and is correlated with poor patient prognosis. Knockdown of hsa_circ_0046701 expression could inhibit the proliferation, migration and invasion of glioma U251cells.
[Abstract] Objective: To investigate the expression of circular RNA hsa_circ_0046701 in glioma tissues and its effect on the proliferation, migration and invasion of glioma U251 cells. Methods: Tumor tissue specimens and clinical data of fifty-two glioma patients treated surgically in Putuo People's Hospital Affiliated to Tongji University between June 2022 and March 2023 were collected, and another 30 normal brain tissue specimens were collected as controls. The expression level of hsa_circ_0046701 in glioma tissues was detected by qPCR to analyze the relationship between the level and clinical characteristics of the patient. Kaplan-Meier method was used to analyze the relationship between hsa_circ_0046701 level and survival prognosis. Using RNA interference technology, circ_0046701 overexpression and empty vector, siRNA-circ_0046701 and negative control (si-NC) plasmid were transfected into glioma U251 cells, respectively. The experiment cells were divided into the circ 0046701 OE group, Vector group, si-circ_0046701 group and si-NC group. CCK-8 method and Transwell assay were applied to detect the proliferation, migration and invasion abilities of cells in each group. Western blotting was applied to detect the expressions of vimentin, Snail, E-cadherin and cyclin D1 proteins in cells of each group. Results: The expression level of hsa_circ_0046701 in glioma tissues was significantly higher than that in normal brain tissues (P < 0.01). The percentage of patients with WHO glioma grading (grades Ⅲ~Ⅳ) in the hsa_circ_0046701 high-expression group was significantly higher than that of the hsa_circ_0046701 low expression group (P < 0.01). The OS of patients in the high expression group was significantly shorter than that of the low-expression group. Compared with those in the si-NC group, the proliferation ability of U251 cells in the si-circ_0046701 group was significantly reduced (P < 0.05 or P < 0.01), and the numbers of migrated and invaded cells decreased significantly (both P < 0.01). The expressions of vimentin, Snail, and cyclin D1 proteins in the cells was significantly reduced (all P < 0.01), while the expression of E-cadherin protein increased significantly (P < 0.01). Compared with those in the Vector group, the proliferation ability of U251cells in the circ_0046701 OE group increased significantly (P < 0.01); the numbers of migrated and invaded cells increased significantly (both P < 0.01); the expressions of vimentin, Snail, and cyclin D1 proteins in the cells increaseds significantly (all P < 0.01), and the expression of E-cadherin protein decreased significantly (P < 0.01). Conclusion: Circular RNA hsa_circ_0046701 is highly expressed in glioma tissues, and is correlated with poor patient prognosis. Knockdown of hsa_circ_0046701 expression could inhibit the proliferation, migration and invasion of glioma U251cells.
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2012,19(5):550-555, DOI: 10.3872/j.issn.1007-385X.2012.5.018
Abstract:
骨髓增生异常综合征（myelodysplastic syndrome，MDS）的发病机制涉及多阶段、多因素，基因改变与表观遗传修饰可能共同参与了这一过程。DNA甲基化是表观遗传学中一种最为重要的修饰，MDS患者常表现为总体DNA高甲基化。使用DNA甲基转移酶（DNA methyltransferase，DNMT）抑制剂降低总体甲基化水平，在MDS患者中取得了富有成效的临床反应及血液学改善。DNMT抑制剂可分为两类：5-氮杂胞苷(5-azacytidine, 5-Aza-CdR)、地西他滨（5-Aza-2-deoxycytidine, decitabine）等核苷和核苷衍生物类抑制剂，它们可提高MDS患者的临床完全反应率、部分反应率及血液学改善，但缓解率、疗效尚不够令人满意；肼苯哒嗪等非核苷类抑制剂。非核苷类抑制剂与丙戊酸镁联合应用治疗MDS获得成功，为MDS去甲基化治疗药物的研究开启了一种新思路。
骨髓增生异常综合征（myelodysplastic syndrome，MDS）的发病机制涉及多阶段、多因素，基因改变与表观遗传修饰可能共同参与了这一过程。DNA甲基化是表观遗传学中一种最为重要的修饰，MDS患者常表现为总体DNA高甲基化。使用DNA甲基转移酶（DNA methyltransferase，DNMT）抑制剂降低总体甲基化水平，在MDS患者中取得了富有成效的临床反应及血液学改善。DNMT抑制剂可分为两类：5-氮杂胞苷(5-azacytidine, 5-Aza-CdR)、地西他滨（5-Aza-2-deoxycytidine, decitabine）等核苷和核苷衍生物类抑制剂，它们可提高MDS患者的临床完全反应率、部分反应率及血液学改善，但缓解率、疗效尚不够令人满意；肼苯哒嗪等非核苷类抑制剂。非核苷类抑制剂与丙戊酸镁联合应用治疗MDS获得成功，为MDS去甲基化治疗药物的研究开启了一种新思路。
2016,23(2):149-160, DOI: 10.3872/j.issn.1007-385X.2016.02.001
Abstract:
Immunocyte therapy for tumor has drawn a great attention in recent years due to its significant effect. Immunocytes, including T cell, NK cell and DCs, play a key role in immune responses of anti-tumors and immunotherapy of tumors. Among them, the techique of chimeric antigen receptor (CAR) modified-T cell (CAR-T) and inhibitor therapy which reverses CTLA-4 and PD-1/PD-L1 and so on immune checkpoints of tumor immune suppressive function have respectively achieved exciting results in therapies of blood tumors, melanoma and other solid tumors. How to further improve the efficacy, to increase adaptive tumor diseases and to control immune related adverse reactions of the therapy could become the focus of future research. NK cell will also take advantages of CAR technique and inhibitors of immune checkpoints to further strengthen its role in the tumor therapy. How to enhance the curative effect of DCs as the first therapeutic tumor vaccine approved by FDA based on its confirmed safe and non-toxic side effects could become a hot point. In this paper, problems that need to be solved in the field were further analyzed and prospected with combination of recent advances in the immunocyte-therapy for tumor.
Immunocyte therapy for tumor has drawn a great attention in recent years due to its significant effect. Immunocytes, including T cell, NK cell and DCs, play a key role in immune responses of anti-tumors and immunotherapy of tumors. Among them, the techique of chimeric antigen receptor (CAR) modified-T cell (CAR-T) and inhibitor therapy which reverses CTLA-4 and PD-1/PD-L1 and so on immune checkpoints of tumor immune suppressive function have respectively achieved exciting results in therapies of blood tumors, melanoma and other solid tumors. How to further improve the efficacy, to increase adaptive tumor diseases and to control immune related adverse reactions of the therapy could become the focus of future research. NK cell will also take advantages of CAR technique and inhibitors of immune checkpoints to further strengthen its role in the tumor therapy. How to enhance the curative effect of DCs as the first therapeutic tumor vaccine approved by FDA based on its confirmed safe and non-toxic side effects could become a hot point. In this paper, problems that need to be solved in the field were further analyzed and prospected with combination of recent advances in the immunocyte-therapy for tumor.
2018,25(1):23-27, DOI: 10.3872/j.issn.1007-385X.2018.01.004
Abstract:
Prostate cancer has become one of the most common malignant diseases in Chinese male. Hormonal therapy is an important and effective way to treat prostate cancer (especially advanced prostate cancer); however, some disputes merged from the clinical application are still to be solved. It seems crucial to unify the understanding and implement overall management to get satisfied effect in hormonal therapy of prostate cancer. According to guidelines and clinical trials in both domestic and overseas, we make a summary of series of problems that appeared in hormonal therapy of prostate cancer, such as treatment opportunity, treatment strategy, patients choose, prognosis and follow-up etc.
Prostate cancer has become one of the most common malignant diseases in Chinese male. Hormonal therapy is an important and effective way to treat prostate cancer (especially advanced prostate cancer); however, some disputes merged from the clinical application are still to be solved. It seems crucial to unify the understanding and implement overall management to get satisfied effect in hormonal therapy of prostate cancer. According to guidelines and clinical trials in both domestic and overseas, we make a summary of series of problems that appeared in hormonal therapy of prostate cancer, such as treatment opportunity, treatment strategy, patients choose, prognosis and follow-up etc.
2010,17(1):57-61, DOI: 10.3872/j.issn.1007-385X.2010.1.011
Abstract:
Objective: To prepare poly DL lactide poly (PELA) microspheres encapsulating recombinant tissue inhibitors of metalloproteinase 1 (TIMP 1) adenovirus, and to investigate their effects on the proliferation of hepatocellular carcinoma HepG2 cells. Methods:The microsphere was constructed by encapsulating recombinant adenovirus containing TIMP 1 in biodegradable PELA. The diameter of the microsphere, quantity of virus encapsulated, loading rate, and releasing kinetics were measured. HepG2 cells were infected with the microspheres; the infection efficiency was examined by fluorescent microscope; and the ultrastructure was observed by TEM. The expression of TIMP 1 mRNA in HepG2 cells was examined by semi quantitative RT PCR, and the proliferation of HepG2 cells was detected by MTT assay. Results:The microsphere encapsulating recombinant TIMP 1 adenovirus was successfully constructed, with its diameter, entrapment efficiency, and virus loading rate being 1.965, 60.0%, and 10.5×108/mg, respectively. About 60% of the viruses were released within 120 h, and the total releasing time was longer than 240 h. Infection with rAdTIMP 1 PELA microsphere efficiently induced TIMP 1 expression in HepG2 cells, and significantly inhibited the proliferation of HepG2 cells, with the inhibitory rate being 47%. Conclusion:PELA microsphere encapsulating recombinant TIMP 1 adenovirus can markedly inhibit the proliferation of HepG2 cells, which provides an experimental basis for the combining macromolecular chemistry and gene therapy for treatment of hepatocellular carcinoma.
Objective: To prepare poly DL lactide poly (PELA) microspheres encapsulating recombinant tissue inhibitors of metalloproteinase 1 (TIMP 1) adenovirus, and to investigate their effects on the proliferation of hepatocellular carcinoma HepG2 cells. Methods:The microsphere was constructed by encapsulating recombinant adenovirus containing TIMP 1 in biodegradable PELA. The diameter of the microsphere, quantity of virus encapsulated, loading rate, and releasing kinetics were measured. HepG2 cells were infected with the microspheres; the infection efficiency was examined by fluorescent microscope; and the ultrastructure was observed by TEM. The expression of TIMP 1 mRNA in HepG2 cells was examined by semi quantitative RT PCR, and the proliferation of HepG2 cells was detected by MTT assay. Results:The microsphere encapsulating recombinant TIMP 1 adenovirus was successfully constructed, with its diameter, entrapment efficiency, and virus loading rate being 1.965, 60.0%, and 10.5×108/mg, respectively. About 60% of the viruses were released within 120 h, and the total releasing time was longer than 240 h. Infection with rAdTIMP 1 PELA microsphere efficiently induced TIMP 1 expression in HepG2 cells, and significantly inhibited the proliferation of HepG2 cells, with the inhibitory rate being 47%. Conclusion:PELA microsphere encapsulating recombinant TIMP 1 adenovirus can markedly inhibit the proliferation of HepG2 cells, which provides an experimental basis for the combining macromolecular chemistry and gene therapy for treatment of hepatocellular carcinoma.
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Chinese Journal Of Cancer Biotheray ® 2025 All Rights Reserved
Supported by:Beijing E-Tiller Technology Development Co., Ltd.
Chinese Journal Of Cancer Biotheray ® 2025 All Rights Reserved
Supported by:Beijing E-Tiller Technology Development Co., Ltd.