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Volume 27,Issue 10,2020 Table of Contents
2020, 27(10):1073-1080.
DOI: 10.3872/j.issn.1007-385X.2020.10.001
Abstract:
Myeloid-derived suppressor cells (MDSCs) are a group of highly heterogeneous immunosuppressive cells produced in the bone marrow, which accumulate in large amounts under pathological conditions such as malignant tumors. MDSCs are the significant cell subsets that reduce patients' response to traditional treatment and promote tumor progression. In recent years, immune checkpoint blockade and adoptive transfusion of engineered T cells have significantly prolonged the survival of many patients with advanced malignant tumors, but the effective rate from 15% to 40% in some solid tumors including lung cancer, colorectal cancer etc., which is closely related to the immunosuppressive microenvironment in solid cancers. With the accumulation in tumor microenvironment, MDSCs reduce the anti-tumor immune response of patients by inhibiting T cell or NK cell proliferation and function, which is the key mechanism for patients tolerating to immunotherapy. Therefore, clarifying the accumulation and functional characteristics of MDSCs is an important research direction to explore the improvement of restoring immunotherapy. This article will systematically elaborate the regulatory mechanism of MDSC production, aggregation and immunosuppressive function, and outline the latest research progress of targeted MDSC therapy.
Myeloid-derived suppressor cells (MDSCs) are a group of highly heterogeneous immunosuppressive cells produced in the bone marrow, which accumulate in large amounts under pathological conditions such as malignant tumors. MDSCs are the significant cell subsets that reduce patients' response to traditional treatment and promote tumor progression. In recent years, immune checkpoint blockade and adoptive transfusion of engineered T cells have significantly prolonged the survival of many patients with advanced malignant tumors, but the effective rate from 15% to 40% in some solid tumors including lung cancer, colorectal cancer etc., which is closely related to the immunosuppressive microenvironment in solid cancers. With the accumulation in tumor microenvironment, MDSCs reduce the anti-tumor immune response of patients by inhibiting T cell or NK cell proliferation and function, which is the key mechanism for patients tolerating to immunotherapy. Therefore, clarifying the accumulation and functional characteristics of MDSCs is an important research direction to explore the improvement of restoring immunotherapy. This article will systematically elaborate the regulatory mechanism of MDSC production, aggregation and immunosuppressive function, and outline the latest research progress of targeted MDSC therapy.
2020, 27(10):1081-1086.
DOI: 10.3872/j.issn.1007-385X.2020.10.002
Abstract:
Objective: To investigate the effect of 18H12, a functional monoclonal antibody that can target gastric cancer stem cells, on the self-renewal and invasion ability of gastric cancer cells. Methods: The gastric cancer cell line PAMC-82 was used as cell model, the expression of ENO1 (enolase-1) on the membrane surface of its parental cells and enriched stem cells by sphere culture was detected by Flow cytometry.Flowcytometrywasusedtoseparate ENO1+ cells and ENO1-cellstodetecttheirself-renewal ability and invasion ability. With the commercial ENO1 antigen and antibody as the samples, CoIP (co-immunoprecipitation) was used to verify whether 18H12 antibody targeting ENO1 could able to accurately recognize ENO1. After being treated with 18H12 for 12 h, 24 h and 48 h, the selfrenewal and invasion ability of PAMC-82 cells were detected by methylcellulose pelletization experiment and Transwell chamber assay, respectively. Results: Flow cytometry showed that the expression of ENO1 on the membrane surface of PAMC-82 sphere cells was significantly higher than that of its parental cells (P<0.01), so ENO1 could be a potential target for targeting gastric cancer stem cells. The self-renewal ability and invasion ability of the sorted ENO1+ cells were significantly stronger than those of the ENO1cells and the parental cells (P<0.05 or P<0.01). 18H12 antibody could accurately recognize ENO1, which was consistent with the commercial antibody recognition band. 18H12 could significantly inhibit self-renewal ability and invasion ability of PAMC-82 cells (P<0.01). Conclusion: Monoclonal antibody 18H12 can significantly inhibit the self-renewal and invasion of gastric cancer stem cells and is expected to be a candidate antibody drug targeting gastric cancer stem cells.
Objective: To investigate the effect of 18H12, a functional monoclonal antibody that can target gastric cancer stem cells, on the self-renewal and invasion ability of gastric cancer cells. Methods: The gastric cancer cell line PAMC-82 was used as cell model, the expression of ENO1 (enolase-1) on the membrane surface of its parental cells and enriched stem cells by sphere culture was detected by Flow cytometry.Flowcytometrywasusedtoseparate ENO1+ cells and ENO1-cellstodetecttheirself-renewal ability and invasion ability. With the commercial ENO1 antigen and antibody as the samples, CoIP (co-immunoprecipitation) was used to verify whether 18H12 antibody targeting ENO1 could able to accurately recognize ENO1. After being treated with 18H12 for 12 h, 24 h and 48 h, the selfrenewal and invasion ability of PAMC-82 cells were detected by methylcellulose pelletization experiment and Transwell chamber assay, respectively. Results: Flow cytometry showed that the expression of ENO1 on the membrane surface of PAMC-82 sphere cells was significantly higher than that of its parental cells (P<0.01), so ENO1 could be a potential target for targeting gastric cancer stem cells. The self-renewal ability and invasion ability of the sorted ENO1+ cells were significantly stronger than those of the ENO1cells and the parental cells (P<0.05 or P<0.01). 18H12 antibody could accurately recognize ENO1, which was consistent with the commercial antibody recognition band. 18H12 could significantly inhibit self-renewal ability and invasion ability of PAMC-82 cells (P<0.01). Conclusion: Monoclonal antibody 18H12 can significantly inhibit the self-renewal and invasion of gastric cancer stem cells and is expected to be a candidate antibody drug targeting gastric cancer stem cells.
2020, 27(10):1087-1092.
DOI: 10.3872/j.issn.1007-385X.2020.10.003
Abstract:
Objective: To investigate the effect of lncRNA SNHG15 targeting miR-153 on cell viability and apoptosis of breast cancer cells and its apoptotic mechanism.Methods:The expression of SNHG15 in breastcancercelllines(MDA-MB-231, BT-549 and MCF-7) were detected by Real-time fluorescent quantitative PCR (qPCR). MDA-MB-231 cells were divided into control (Ctrl) group, si-NC group, si-SNHG15 group, si-SNHG15+anti-NC group and si-SNHG15+anti-miR-153 group. Cell viability and apoptosis rate were detected by MTT and Flow cytometry, respectively. The targeting relationship between SNHG15 and miR-153 was verified by Dual luciferase report gene system. Mitochondrial membrane potential fluorescent probe (JC-1) staining method was used to detect cell mitochondrial membrane potential.The expressions of mitochondrial apoptosis-related proteins (Bcl-2, Bax, caspase3, cleaved caspase3 [c-caspase3] and Cyt-C）were detected by Western blotting. Results:TheexpressionofSNHG15 in breast cancer cells was significantly higher than that in human normal mammary epithelial MCF10A cells (P<0.01). There was a targeting relationship between SNHG15 and miR-153. Compared with the control group, the cell viability and mitochondrial membrane potential of MDA-MB-231 cells in si-SNHG15 group were decreased, while apoptosis rate was increased (all P<0.01); the expressions of Bcl-2 and caspase3 were decreased while expressions of Bax, c-caspase3 and Cyt-C were increased (all P<0.01). However, co-transfection of si-SNHG15 and anti-miR-153 significantly attenuated the effects of si-SNHG15 on cell viability, apoptosis, mitochondrial membrane potential and expressions of Bcl-2, Bax, caspase3, c-caspase3 and Cyt-C (all P<0.01). Conclusion: lncRNA SNHG15 can target miR-153 to induce apoptosis of MDA-MB-231 cells, and the mechanism may be related to the regulation of apoptosis of mitochondrial pathway.
Objective: To investigate the effect of lncRNA SNHG15 targeting miR-153 on cell viability and apoptosis of breast cancer cells and its apoptotic mechanism.Methods:The expression of SNHG15 in breastcancercelllines(MDA-MB-231, BT-549 and MCF-7) were detected by Real-time fluorescent quantitative PCR (qPCR). MDA-MB-231 cells were divided into control (Ctrl) group, si-NC group, si-SNHG15 group, si-SNHG15+anti-NC group and si-SNHG15+anti-miR-153 group. Cell viability and apoptosis rate were detected by MTT and Flow cytometry, respectively. The targeting relationship between SNHG15 and miR-153 was verified by Dual luciferase report gene system. Mitochondrial membrane potential fluorescent probe (JC-1) staining method was used to detect cell mitochondrial membrane potential.The expressions of mitochondrial apoptosis-related proteins (Bcl-2, Bax, caspase3, cleaved caspase3 [c-caspase3] and Cyt-C）were detected by Western blotting. Results:TheexpressionofSNHG15 in breast cancer cells was significantly higher than that in human normal mammary epithelial MCF10A cells (P<0.01). There was a targeting relationship between SNHG15 and miR-153. Compared with the control group, the cell viability and mitochondrial membrane potential of MDA-MB-231 cells in si-SNHG15 group were decreased, while apoptosis rate was increased (all P<0.01); the expressions of Bcl-2 and caspase3 were decreased while expressions of Bax, c-caspase3 and Cyt-C were increased (all P<0.01). However, co-transfection of si-SNHG15 and anti-miR-153 significantly attenuated the effects of si-SNHG15 on cell viability, apoptosis, mitochondrial membrane potential and expressions of Bcl-2, Bax, caspase3, c-caspase3 and Cyt-C (all P<0.01). Conclusion: lncRNA SNHG15 can target miR-153 to induce apoptosis of MDA-MB-231 cells, and the mechanism may be related to the regulation of apoptosis of mitochondrial pathway.
YE Wangzhong
,
XU Yuanji
,
YE Yunbin
,
HUANG Xinyi
,
LIU Fang
,
LI Jieyu
,
LIN Zhizhong
,
BAI Penggang
,
CHEN Chuanben
2020, 27(10):1093-1099.
DOI: 10.3872/j.issn.1007-385X.2020.10.004
Abstract:
Objective: To explore the role of adhesion molecule with Ig like domain 2 (AMIGO2) in the proliferation of nasopharyngeal carcinoma (NPC) cells and its mechanisms. Methods: A total of 10 NPC tissue samples and 10 normal nasopharyngeal epithelial tissue samples collected at Fujian Cancer Hospital during September 2017 and November 2017 were used for this study; in addition, NPC cell lines (CNE-1, CNE-2, SUNE-1, 6-10B, C666-1) and human immobilized nasopharyngeal epithelial cell line NP69 were also collected. The relative expressionofAMIGO2mRNAinabovementionedtissuesandcelllineswasdetectedby qPCR. Lentivirus vectors were constructed to interfere AMIGO2 mRNA expression, and qPCR was used to verify its interference efficiency. CCK-8 method, Clonal formation and Flow cytometry were performed to evaluate the effect of AMIGO2 interference on proliferation, clone formation and apoptosis of NPC cells. The influence ofAMIGO2 interference on PI3K/AKT/mTOR signaling pathway and proliferation related molecular markers in NPC cells was assessed by Western blotting. Results: The results of qPCR showed that AMIGO2 was highly expressed in NPC tissues, CNE-2, and SUNE-1 cells (all P<0.01). The interference efficiency of AMIGO2 in CNE-2 and SUNE-1 cells could reach over 50%. The interfering of AMIGO2 expression significantly inhibited the proliferation and clone formation of CNE-2 and SUNE-1 cells (all P<0.01), promoted cell apoptosis (all P<0.01), reduced the phosphorylated protein expression levels of PI3K, AKT and mTOR in SUNE-1 cells (all P<0.01), as well as down-regulated the protein expressions of survivin and PCNA (all P<0.01). Conclusion: AMIGO2 may promote the proliferation as well as inhibit apoptosis of NPC cells by activating the PI3K/AKT/mTOR signaling pathway, suggesting thatAMIGO2 may be a potential target for NPC therapy.
Objective: To explore the role of adhesion molecule with Ig like domain 2 (AMIGO2) in the proliferation of nasopharyngeal carcinoma (NPC) cells and its mechanisms. Methods: A total of 10 NPC tissue samples and 10 normal nasopharyngeal epithelial tissue samples collected at Fujian Cancer Hospital during September 2017 and November 2017 were used for this study; in addition, NPC cell lines (CNE-1, CNE-2, SUNE-1, 6-10B, C666-1) and human immobilized nasopharyngeal epithelial cell line NP69 were also collected. The relative expressionofAMIGO2mRNAinabovementionedtissuesandcelllineswasdetectedby qPCR. Lentivirus vectors were constructed to interfere AMIGO2 mRNA expression, and qPCR was used to verify its interference efficiency. CCK-8 method, Clonal formation and Flow cytometry were performed to evaluate the effect of AMIGO2 interference on proliferation, clone formation and apoptosis of NPC cells. The influence ofAMIGO2 interference on PI3K/AKT/mTOR signaling pathway and proliferation related molecular markers in NPC cells was assessed by Western blotting. Results: The results of qPCR showed that AMIGO2 was highly expressed in NPC tissues, CNE-2, and SUNE-1 cells (all P<0.01). The interference efficiency of AMIGO2 in CNE-2 and SUNE-1 cells could reach over 50%. The interfering of AMIGO2 expression significantly inhibited the proliferation and clone formation of CNE-2 and SUNE-1 cells (all P<0.01), promoted cell apoptosis (all P<0.01), reduced the phosphorylated protein expression levels of PI3K, AKT and mTOR in SUNE-1 cells (all P<0.01), as well as down-regulated the protein expressions of survivin and PCNA (all P<0.01). Conclusion: AMIGO2 may promote the proliferation as well as inhibit apoptosis of NPC cells by activating the PI3K/AKT/mTOR signaling pathway, suggesting thatAMIGO2 may be a potential target for NPC therapy.
2020, 27(10):1100-1105.
DOI: 10.3872/j.issn.1007-385X.2020.10.005
Abstract:
Objective: To investigate the miR-423-5p expression in brain glioma tissues and cell lines, and its promotive effect on temozolomide (TMZ) chemoresistance by targeting PDCD5 (programmed cell death protein 5). Methods: Tumor tissues and matched peritumoral tissues were collected from 20 brain glioma patients who were surgically treated in the Department of Neurosurgery, Affiliated Hospital of Beihua University between January 2017 and December 2018. Glioblastoma cell lines (U251, U87, SHG-44) and human normal glial cell line HMC-3 were also used in the study. The relative expression of miR-423-5p and PDCD5 in brain glioma and peritumoral tissues andcelllineswasdetected by qPCR.ThesynthesizedmiR-423-5p mimics and miR-NC were respectively transfected into U251 and U87 cells; meanwhile,TMZatdifferentconcentrations (50, 100, 150 and 200 μmol/L) werealsousedtotreat thecells. Then, the chemoresistance of cells to TMZ were determined. MTT assayandcolonyformationassaywereusedtoexaminethe proliferationofU251andU87cells,andWesternblotting was used to detect the expression of c-caspase 3, Bcl-2 and PDCD5 proteins in U251 and U87 cells. The targeting relationship between PDCD5 and miR-423-5p was validated through Dual luciferasereportergene assay. Results: miR-423-5p was highly expressed in glioma tissues and glioma cell lines (all P<0.01). As compared with the miR-NC group, the proliferation and TMZ-chemoresistance of U251 and U87 cells in miR-423-5p mimics group significantly increased (all P<0.01). Dual luciferase reporter gene assay validated that miR-423-5p could bind with PDCD5 3' UTR to suppress the expression of PDCD5. Conclusion: High expression of miR-423-5p enhances the chemoresistance of glioma cells to TMZ, and miR-423-5p may serve as a potential therapeutic target in the treatment of brain glioma.
Objective: To investigate the miR-423-5p expression in brain glioma tissues and cell lines, and its promotive effect on temozolomide (TMZ) chemoresistance by targeting PDCD5 (programmed cell death protein 5). Methods: Tumor tissues and matched peritumoral tissues were collected from 20 brain glioma patients who were surgically treated in the Department of Neurosurgery, Affiliated Hospital of Beihua University between January 2017 and December 2018. Glioblastoma cell lines (U251, U87, SHG-44) and human normal glial cell line HMC-3 were also used in the study. The relative expression of miR-423-5p and PDCD5 in brain glioma and peritumoral tissues andcelllineswasdetected by qPCR.ThesynthesizedmiR-423-5p mimics and miR-NC were respectively transfected into U251 and U87 cells; meanwhile,TMZatdifferentconcentrations (50, 100, 150 and 200 μmol/L) werealsousedtotreat thecells. Then, the chemoresistance of cells to TMZ were determined. MTT assayandcolonyformationassaywereusedtoexaminethe proliferationofU251andU87cells,andWesternblotting was used to detect the expression of c-caspase 3, Bcl-2 and PDCD5 proteins in U251 and U87 cells. The targeting relationship between PDCD5 and miR-423-5p was validated through Dual luciferasereportergene assay. Results: miR-423-5p was highly expressed in glioma tissues and glioma cell lines (all P<0.01). As compared with the miR-NC group, the proliferation and TMZ-chemoresistance of U251 and U87 cells in miR-423-5p mimics group significantly increased (all P<0.01). Dual luciferase reporter gene assay validated that miR-423-5p could bind with PDCD5 3' UTR to suppress the expression of PDCD5. Conclusion: High expression of miR-423-5p enhances the chemoresistance of glioma cells to TMZ, and miR-423-5p may serve as a potential therapeutic target in the treatment of brain glioma.
2020, 27(10):1106-1111.
DOI: 10.3872/j.issn.1007-385X.2020.10.006
Abstract:
Objective: To investigate the effects of silencing monocarboxylate transporter 4 (MCT4) on the proliferation, migration and invasion of prostate cancer PC3 cells and its possible molecular mechanism. Methods: RNA interference technology was used to transfect siRNA-MCT4 (si-MCT4) and negative control plasmid (si-NC) into PC3 cells, respectively. The content of lactic acid in the cell culture medium of transfected PC3 cells was detected by lactic acid assay after culturing for 96 h. The proliferation, migration and invasion abilityofPC3cellsweredetectedbyCCK-8andTranswellassay,respectively. Western blotting was used to detect the silencing effect and the expressions of integrin β4-FAK-SRC-MEK-ERK signaling pathway associated proteins (integrin β4, p-FAK, p-SRC, p-ERK1/2, p-MEK1/2) and EMT associated proteins (E-cadherin and N-cadherin). Results: PC3 cell line with silenced MCT4 was successfully constructed. Compared with the control group, the content of extracellular lactic acid in the PC3 cell culture medium of the si-MCT4 group was significantly decreased (P<0.01), and the proliferation, migration and invasion of cells were significantly decreased (P<0.05 or P<0.01). Compared with the control group, the protein expressions of integrin β4, p-FAK, p-SRC, p-MEK1/2, p-ERK1/2 and N-cadherin were significantly decreased (all P<0.01), while the protein expression of E-cadherin was significantly increased (P<0.01). Conclusion: Silencing MCT4 can significantly inhibit the proliferation, migration and invasion of PC3 cells, the mechanism of which may be related to the inhibition of lactic acid level in cell culture medium and suppression of integrin β4-FAK-SRC-MEKERK signaling pathway associated proteins as well as EMT associated proteins.
Objective: To investigate the effects of silencing monocarboxylate transporter 4 (MCT4) on the proliferation, migration and invasion of prostate cancer PC3 cells and its possible molecular mechanism. Methods: RNA interference technology was used to transfect siRNA-MCT4 (si-MCT4) and negative control plasmid (si-NC) into PC3 cells, respectively. The content of lactic acid in the cell culture medium of transfected PC3 cells was detected by lactic acid assay after culturing for 96 h. The proliferation, migration and invasion abilityofPC3cellsweredetectedbyCCK-8andTranswellassay,respectively. Western blotting was used to detect the silencing effect and the expressions of integrin β4-FAK-SRC-MEK-ERK signaling pathway associated proteins (integrin β4, p-FAK, p-SRC, p-ERK1/2, p-MEK1/2) and EMT associated proteins (E-cadherin and N-cadherin). Results: PC3 cell line with silenced MCT4 was successfully constructed. Compared with the control group, the content of extracellular lactic acid in the PC3 cell culture medium of the si-MCT4 group was significantly decreased (P<0.01), and the proliferation, migration and invasion of cells were significantly decreased (P<0.05 or P<0.01). Compared with the control group, the protein expressions of integrin β4, p-FAK, p-SRC, p-MEK1/2, p-ERK1/2 and N-cadherin were significantly decreased (all P<0.01), while the protein expression of E-cadherin was significantly increased (P<0.01). Conclusion: Silencing MCT4 can significantly inhibit the proliferation, migration and invasion of PC3 cells, the mechanism of which may be related to the inhibition of lactic acid level in cell culture medium and suppression of integrin β4-FAK-SRC-MEKERK signaling pathway associated proteins as well as EMT associated proteins.
2020, 27(10):1112-1117.
DOI: 10.3872/j.issn.1007-385X.2020.10.007
Abstract:
Objective: To investigate the expression of MAGE-C1 (melanoma-associated antigen-C1) in breast cancer tissues and its correlation with clinicopathological features and prognosis of breast cancer patients. Methods: Breast cancer tissues, normal breast tissues and benign breast lesion tissues (60 samples for each) were collected from the Fourth Hospital of Hebei Medical University during January2008andDecember2008.ThemRNAand protein expressions of MAGE-C1 in three types of breast tissues were detected by RT-PCR and immunohistochemistry, and their correlation with clinicopathological parameters and prognosis of breast cancer patients were also analyzed. DNAmethylaseinhibitor5-aza-2'-deoxycytidine(5-Aza-CdR)and histone deacetylase inhibitor trichostatin A (TSA) were used to treat breast cancer MDA-MB-231 and MCF-7 cells, and RT-PCR was used to determine the changes in mRNA expression of MAGE-C1 after drug treatment. Results: The positive expression rate of MAGE-C1 mRNA and protein in breast cancer tissues were 43.3% (26/60) and 38.3% (23/60), respectively; and the mRNA and protein expressions of MAGE-C1 were all negative in normal breast tissues and benign breast lesion tissues. MAGE-C1 expression was positively associated with high tumor grade (χ2=6.233, P<0.05). Recurrence-free survival (RFS) of patients with negative MAGE-C1 expression was significantly longer than those patients with positive MAGE-C1 expression (χ2=4.213, P<0.05). MAGE-C1 expression (HR=3.980, P<0.05) and clinical stage (HR=3.637, P<0.05) could be used as independent prognostic factors for breast cancer patients. 5-Aza-CdR and/or TSA treatment had no significant influence on MAGE-C1 gene expression (P>0.05). Conclusion: MAGE-C1 is a tumor-specific antigen and its expression is associated with poor prognosis of breast cancer patients.
Objective: To investigate the expression of MAGE-C1 (melanoma-associated antigen-C1) in breast cancer tissues and its correlation with clinicopathological features and prognosis of breast cancer patients. Methods: Breast cancer tissues, normal breast tissues and benign breast lesion tissues (60 samples for each) were collected from the Fourth Hospital of Hebei Medical University during January2008andDecember2008.ThemRNAand protein expressions of MAGE-C1 in three types of breast tissues were detected by RT-PCR and immunohistochemistry, and their correlation with clinicopathological parameters and prognosis of breast cancer patients were also analyzed. DNAmethylaseinhibitor5-aza-2'-deoxycytidine(5-Aza-CdR)and histone deacetylase inhibitor trichostatin A (TSA) were used to treat breast cancer MDA-MB-231 and MCF-7 cells, and RT-PCR was used to determine the changes in mRNA expression of MAGE-C1 after drug treatment. Results: The positive expression rate of MAGE-C1 mRNA and protein in breast cancer tissues were 43.3% (26/60) and 38.3% (23/60), respectively; and the mRNA and protein expressions of MAGE-C1 were all negative in normal breast tissues and benign breast lesion tissues. MAGE-C1 expression was positively associated with high tumor grade (χ2=6.233, P<0.05). Recurrence-free survival (RFS) of patients with negative MAGE-C1 expression was significantly longer than those patients with positive MAGE-C1 expression (χ2=4.213, P<0.05). MAGE-C1 expression (HR=3.980, P<0.05) and clinical stage (HR=3.637, P<0.05) could be used as independent prognostic factors for breast cancer patients. 5-Aza-CdR and/or TSA treatment had no significant influence on MAGE-C1 gene expression (P>0.05). Conclusion: MAGE-C1 is a tumor-specific antigen and its expression is associated with poor prognosis of breast cancer patients.
2020, 27(10):1118-1125.
DOI: 10.3872/j.issn.1007-385X.2020.10.008
Abstract:
Objective: To investigate the expression level of lncRNA (long non-coding RNA) SNHG1 in endometrial cancer tissues, and to analyze its mechanism of action as well as its clinical significance. Methods: NCBI-GEO and TCGA database were used to analyze the expression level of SNHG1 in endometrial cancer. A total of 53 cases of endometrial cancer tissue samples and 41 cases of normal endometrial tissuesampleswerecollectedfromJanuary 2016 to March 2019atZhongxin Ecocity Hospital of Tianjin Medical University;inaddition,endometrialcancercelllinesIshikawaandHEC-1AaswellasnormalendometrialESCcellswerealsocollected for thisstudy. qPCR was used to detecttheexpressionlevelofSNHG1intissuesandcells,anditscorrelation with the clinical characteristics of patients were statistically analyzed. The effect of SNHG1 on cell proliferation and apoptosis of HEC-1A cells was measured by MTT assay and Annexin V/PI double staining Flow cytometry, respectively. The migration and invasion of HEC-1A cells were measured by Transwell assay. StarBase was used to predict the regulatory relationship between SNHG1 and RELA, which was then verified by qPCR and Western blotting. Dual fluorescent reporter gene system and qPCR were adopted to identify the influence of SNHG1 on NF-κB pathway. Results: The expression of SNHG1 was significantly up-regulated in endometrial cancer tissues compared with normal endometrial tissues (P<0.01), and its expression was related to tumor size, TNM staging, histological grade and lymph node metastasis (all P<0.05). The expression level of SNHG1 in Ishikawa and HEC-1A cells was significantly higher than that in ESC cells (all P<0.01). Overexpression of SNHG1 notably promoted the proliferation, migration and invasion and inhibited cell apoptosis of HEC-1A cells. By promoting the expression of RELA, SNHG1 activated the NF-κB pathway and promoted the expressions of downstream gene IL-6 and CCL19 (all P<0.01). Conclusion: Up-regulated SNHG1 in endometrial cancer functions as an oncogene by activating the NF-κB pathway through promoting the RELAexpression.
Objective: To investigate the expression level of lncRNA (long non-coding RNA) SNHG1 in endometrial cancer tissues, and to analyze its mechanism of action as well as its clinical significance. Methods: NCBI-GEO and TCGA database were used to analyze the expression level of SNHG1 in endometrial cancer. A total of 53 cases of endometrial cancer tissue samples and 41 cases of normal endometrial tissuesampleswerecollectedfromJanuary 2016 to March 2019atZhongxin Ecocity Hospital of Tianjin Medical University;inaddition,endometrialcancercelllinesIshikawaandHEC-1AaswellasnormalendometrialESCcellswerealsocollected for thisstudy. qPCR was used to detecttheexpressionlevelofSNHG1intissuesandcells,anditscorrelation with the clinical characteristics of patients were statistically analyzed. The effect of SNHG1 on cell proliferation and apoptosis of HEC-1A cells was measured by MTT assay and Annexin V/PI double staining Flow cytometry, respectively. The migration and invasion of HEC-1A cells were measured by Transwell assay. StarBase was used to predict the regulatory relationship between SNHG1 and RELA, which was then verified by qPCR and Western blotting. Dual fluorescent reporter gene system and qPCR were adopted to identify the influence of SNHG1 on NF-κB pathway. Results: The expression of SNHG1 was significantly up-regulated in endometrial cancer tissues compared with normal endometrial tissues (P<0.01), and its expression was related to tumor size, TNM staging, histological grade and lymph node metastasis (all P<0.05). The expression level of SNHG1 in Ishikawa and HEC-1A cells was significantly higher than that in ESC cells (all P<0.01). Overexpression of SNHG1 notably promoted the proliferation, migration and invasion and inhibited cell apoptosis of HEC-1A cells. By promoting the expression of RELA, SNHG1 activated the NF-κB pathway and promoted the expressions of downstream gene IL-6 and CCL19 (all P<0.01). Conclusion: Up-regulated SNHG1 in endometrial cancer functions as an oncogene by activating the NF-κB pathway through promoting the RELAexpression.
2020, 27(10):1126-1130.
DOI: 10.3872/j.issn.1007-385X.2020.10.009
Abstract:
Objective: To investigate the expression of miR-191 in cervical cancer tissues and its effect on the patients' prognosis. Methods: One hundred and seven cervical cancer tissue specimens from patients who underwent surgical treatment and 46 normal cervical tissue specimens from patients who underwent surgical resection of uterine fibroids (the control group) in Xinxiang Central Hospital were collected from December 2012 to December 2014. The expression of miR-191 in cancer tissues was detected by qPCR. All patients were followed up from the first day after surgery, and the follow-up deadline was December 31, 2019. All patients were followed up for 5 years, with death as the end event. The survival time and 5-year survival rate of the patients were recorded. Survival analysis was performed using Kaplan-Meier method and the factors affecting survival prognosis were analyzed using Cox proportional hazard regression model. Results: The expression level of miR-191 in cervical cancer tissues was significantly higher than that in the tissues from control group (P<0.01). There were significant differences in miR-191 expression among patients with different high-risk HPV infection status, different pathological grades and FIGO stages, and different lymph node metastasis status (all P<0.01). The 5-year survival rate of patients in the miR-191 low expression group was significantly higher than those patients in the high expression group (81.48% vs 33.75%, χ2=16.905, P<0.01). Pathological grade, FIGO stage, lymph node metastasis and the expression of miR-191 were risk factors affecting the prognosis of cervical cancer patients (HR=0.486, 3.065, 2.339 and 2.755, all P<0.05). Conclusion: miR-191 is highly expressed in cervical cancer tissues, and its expression level increases with the progressionof malignancy. It is expected to become a potential biomarker for early diagnosis and prognosis evaluation of cervical cancer.
Objective: To investigate the expression of miR-191 in cervical cancer tissues and its effect on the patients' prognosis. Methods: One hundred and seven cervical cancer tissue specimens from patients who underwent surgical treatment and 46 normal cervical tissue specimens from patients who underwent surgical resection of uterine fibroids (the control group) in Xinxiang Central Hospital were collected from December 2012 to December 2014. The expression of miR-191 in cancer tissues was detected by qPCR. All patients were followed up from the first day after surgery, and the follow-up deadline was December 31, 2019. All patients were followed up for 5 years, with death as the end event. The survival time and 5-year survival rate of the patients were recorded. Survival analysis was performed using Kaplan-Meier method and the factors affecting survival prognosis were analyzed using Cox proportional hazard regression model. Results: The expression level of miR-191 in cervical cancer tissues was significantly higher than that in the tissues from control group (P<0.01). There were significant differences in miR-191 expression among patients with different high-risk HPV infection status, different pathological grades and FIGO stages, and different lymph node metastasis status (all P<0.01). The 5-year survival rate of patients in the miR-191 low expression group was significantly higher than those patients in the high expression group (81.48% vs 33.75%, χ2=16.905, P<0.01). Pathological grade, FIGO stage, lymph node metastasis and the expression of miR-191 were risk factors affecting the prognosis of cervical cancer patients (HR=0.486, 3.065, 2.339 and 2.755, all P<0.05). Conclusion: miR-191 is highly expressed in cervical cancer tissues, and its expression level increases with the progressionof malignancy. It is expected to become a potential biomarker for early diagnosis and prognosis evaluation of cervical cancer.
2020, 27(10):1131-1137.
DOI: 10.3872/j.issn.1007-385X.2020.10.010
Abstract:
Objective: To investigate the effect of apatinib (APA) combined with cisplatin (DDP) on the proliferation, invasion and migration capacity of gastric carcinoma (GC) cells and its molecular mechanism. Methods: Cancer and para-cancerous tissue samples resected from 50 GC patients, who were surgically treated in Wuwei People's Hospital from January 2016 to June 2019, were collected for this study; in addition, GC cell lines MGC803 and SGC7901 were also collected. qPCR was used to detect the HMGA2 expression in tissues and mRNA expressions of molecules related to cell proliferation, migration and invasion in GC cell lines. MGC803 and SGC7901 cells were transfected with pcHMGA2 by liposome transfection technology. After treatment with DDP and APA at different concentrations, the cells were divided into NC, pcHMGA2, pcHMGA2+DDP and pcHMGA2+DDP+APA groups. Protein expression of HMGA2 in GC cells was detected by Western blotting, and proliferation, migration and invasion of the cells were detected by MTT and Transwell assay, respectively. Results: The mRNA expression of HMGA2 in GC tissues was higher than that in para-cancerous tissues (P<0.05), and the survival rate of GC patients in the high expression group was significantly reduced (P<0.01). DDP significantly inhibited the proliferation, invasion and migration of MGC803 and SGC7901 cells (all P<0.01); the proliferation, invasion and migration of MGC803 and SGC7901 cells in DDP+APA group significantly decreased (all P<0.01) as compared with DDP group; APA significantly enhanced the inhibitory effect of DDP on HMGA2 expression in GC cells (P<0.01); APA enhanced the anticancer activity of DDP against GC by down-regulating HMGA2 expression. Conclusion: APA promotes the anticancer activity of DDP against GC, and its molecular mechanism is the promotion of the inhibitory effect of DDP on HMGA2 expression.
Objective: To investigate the effect of apatinib (APA) combined with cisplatin (DDP) on the proliferation, invasion and migration capacity of gastric carcinoma (GC) cells and its molecular mechanism. Methods: Cancer and para-cancerous tissue samples resected from 50 GC patients, who were surgically treated in Wuwei People's Hospital from January 2016 to June 2019, were collected for this study; in addition, GC cell lines MGC803 and SGC7901 were also collected. qPCR was used to detect the HMGA2 expression in tissues and mRNA expressions of molecules related to cell proliferation, migration and invasion in GC cell lines. MGC803 and SGC7901 cells were transfected with pcHMGA2 by liposome transfection technology. After treatment with DDP and APA at different concentrations, the cells were divided into NC, pcHMGA2, pcHMGA2+DDP and pcHMGA2+DDP+APA groups. Protein expression of HMGA2 in GC cells was detected by Western blotting, and proliferation, migration and invasion of the cells were detected by MTT and Transwell assay, respectively. Results: The mRNA expression of HMGA2 in GC tissues was higher than that in para-cancerous tissues (P<0.05), and the survival rate of GC patients in the high expression group was significantly reduced (P<0.01). DDP significantly inhibited the proliferation, invasion and migration of MGC803 and SGC7901 cells (all P<0.01); the proliferation, invasion and migration of MGC803 and SGC7901 cells in DDP+APA group significantly decreased (all P<0.01) as compared with DDP group; APA significantly enhanced the inhibitory effect of DDP on HMGA2 expression in GC cells (P<0.01); APA enhanced the anticancer activity of DDP against GC by down-regulating HMGA2 expression. Conclusion: APA promotes the anticancer activity of DDP against GC, and its molecular mechanism is the promotion of the inhibitory effect of DDP on HMGA2 expression.
2020, 27(10):1138-1143.
DOI: 10.3872/j.issn.1007-385X.2020.10.011
Abstract:
Objective: To investigate the pathogenesis of prostate cancer by analyzing the associated hub gene modules of prostate cancer and identifying key transcription factors and genes that affect these modules. Methods: WGCNA (weighted gene co-expressed network analysis) was used to identify hub gene modules associated with important clinicopathological features of prostate cancer, such as pathological staging, Gleason grading etc. The OPOSSUM online tool was used to analyze the transcription factors enriching and regulating those genes. Pathway enrichment analysis and protein-protein interaction network analysis were used to identify key genes in prostate cancer. Finally, the effects of these genes on clinical features and disease-free survival (DFS) of prostate cancer patients were analyzed. Results: Three hub modules were identified, and they were highly associated with pathologic T stage, pathologic N stage and Gleason grading of prostate cancer, respectively. Further screening revealed 13 key dysregulated transcription factors that participated in the regulation of these three hub modules. The differentially expressed genes regulated by the 13 key transcription factors were significantly enriched in Calcium signaling pathway, cGMP-PKG signaling pathway and cAMP signaling pathway. 14 key genes (PRKG1, PRKG2, CYSLTR2, GRPR, CHRM3, ADCY5, ADRA1D, EDNRA, EDNRB, CYSLTR2, AGTR1, GRPR, GRIA1 and OXT) were at important nodes in the gene network. Among them, the high expression of ADRA1A, PRKG2, CHRM3, ADRA1D and EDN3 significantly extended the DFS of patients with prostate cancer (all P<0.01). Conclusion: ADRA1A, PRKG2, CHRM3, ADRA1D and EDN3 are regulated by key dysregulated transcription factors and highly associated with clinical features of prostate cancer. Their high expressions will significantly prolong the DFS of prostate cancer patients, which may shed light to the discovery of mechanism in prostate adenocarcinoma.
Objective: To investigate the pathogenesis of prostate cancer by analyzing the associated hub gene modules of prostate cancer and identifying key transcription factors and genes that affect these modules. Methods: WGCNA (weighted gene co-expressed network analysis) was used to identify hub gene modules associated with important clinicopathological features of prostate cancer, such as pathological staging, Gleason grading etc. The OPOSSUM online tool was used to analyze the transcription factors enriching and regulating those genes. Pathway enrichment analysis and protein-protein interaction network analysis were used to identify key genes in prostate cancer. Finally, the effects of these genes on clinical features and disease-free survival (DFS) of prostate cancer patients were analyzed. Results: Three hub modules were identified, and they were highly associated with pathologic T stage, pathologic N stage and Gleason grading of prostate cancer, respectively. Further screening revealed 13 key dysregulated transcription factors that participated in the regulation of these three hub modules. The differentially expressed genes regulated by the 13 key transcription factors were significantly enriched in Calcium signaling pathway, cGMP-PKG signaling pathway and cAMP signaling pathway. 14 key genes (PRKG1, PRKG2, CYSLTR2, GRPR, CHRM3, ADCY5, ADRA1D, EDNRA, EDNRB, CYSLTR2, AGTR1, GRPR, GRIA1 and OXT) were at important nodes in the gene network. Among them, the high expression of ADRA1A, PRKG2, CHRM3, ADRA1D and EDN3 significantly extended the DFS of patients with prostate cancer (all P<0.01). Conclusion: ADRA1A, PRKG2, CHRM3, ADRA1D and EDN3 are regulated by key dysregulated transcription factors and highly associated with clinical features of prostate cancer. Their high expressions will significantly prolong the DFS of prostate cancer patients, which may shed light to the discovery of mechanism in prostate adenocarcinoma.
2020, 27(10):1144-1151.
DOI: 10.3872/j.issn.1007-385X.2020.10.012
Abstract:
Objective: To explore the expression of PSME3 (proteasome activator complex subunit 3) in gastric cancer (GC) tissues and its correlation with the prognosis of GC patients, and tofurtheranalyzeitseffect and mechanism in the occurrence and development of GC. Methods: The expression level of PSME3 gene in GC tissues was analyzed with TCGA and UALCAN database. qPCR was used to verify the expression of PSME3 in GC tissues and corresponding adjacent normal tissues that resected from 40 GC patients who were surgically treated in the Fourth Hospital ofHebeiMedicalUniversityfromJanuary2017toDecember 2018. ROC curve and KaplanMeier plotter method were used to analyzethevalueofPSME3mainlyindiagnosingandpredictingtheprognosis of GC patients. The biological processes and pathways that PSME3 involved in were further analyzed. Results: The expression level of PSME3 in GC tissues was significantly higher than that in normal tissues, and it’s high expression was significantly correlated with the tumor stage, pathological subtype, status of lymph node metastasis and Helicobacter pylori infection in GC patients (all P<0.01). PSME3 was also highly expressed in GC tissue samples collected by the qPCR confirmatory detection group (P<0.01). PSME3 could distinguish gastric cancer patients from normal people with an AUC value of 0.808. The overall survival time, the first progression survival time and post progression survival time of the GC patients with low PSME3 expression were longer than those in the patients with high PSME3 expression (all P<0.01). Mechanism research found that PSME3 mainly played an oncogenic role of the development of GC by regulating cell cycle, mTORC1 signaling pathway, PI3K/AKT/mTOR signaling pathway and TGF-β signaling pathway etc. Conclusion: PSME3 is highly expressed in GC tissues, and it is significantly related to the poor prognosis of GC patients. It plays an oncogenic role in the occurrence and development of GC.
Objective: To explore the expression of PSME3 (proteasome activator complex subunit 3) in gastric cancer (GC) tissues and its correlation with the prognosis of GC patients, and tofurtheranalyzeitseffect and mechanism in the occurrence and development of GC. Methods: The expression level of PSME3 gene in GC tissues was analyzed with TCGA and UALCAN database. qPCR was used to verify the expression of PSME3 in GC tissues and corresponding adjacent normal tissues that resected from 40 GC patients who were surgically treated in the Fourth Hospital ofHebeiMedicalUniversityfromJanuary2017toDecember 2018. ROC curve and KaplanMeier plotter method were used to analyzethevalueofPSME3mainlyindiagnosingandpredictingtheprognosis of GC patients. The biological processes and pathways that PSME3 involved in were further analyzed. Results: The expression level of PSME3 in GC tissues was significantly higher than that in normal tissues, and it’s high expression was significantly correlated with the tumor stage, pathological subtype, status of lymph node metastasis and Helicobacter pylori infection in GC patients (all P<0.01). PSME3 was also highly expressed in GC tissue samples collected by the qPCR confirmatory detection group (P<0.01). PSME3 could distinguish gastric cancer patients from normal people with an AUC value of 0.808. The overall survival time, the first progression survival time and post progression survival time of the GC patients with low PSME3 expression were longer than those in the patients with high PSME3 expression (all P<0.01). Mechanism research found that PSME3 mainly played an oncogenic role of the development of GC by regulating cell cycle, mTORC1 signaling pathway, PI3K/AKT/mTOR signaling pathway and TGF-β signaling pathway etc. Conclusion: PSME3 is highly expressed in GC tissues, and it is significantly related to the poor prognosis of GC patients. It plays an oncogenic role in the occurrence and development of GC.
2020, 27(10):1152-1155.
DOI: 10.3872/j.issn.1007-385X.2020.10.013
Abstract:
Objective: To investigate the short-term clinical efficacy and safety of intraperitoneal perfusion of natural killer (NK) cells in the treatment of ovarian cancer with ascites. Methods: The clinical data of 15 ovarian cancer patients with ascites effusion, who received NK cell perfusion in the Qinhuai Medical District of the General Hospital of Eastern Theater Command from November 2016 to January 2019, were analyzed. The peripheral blood was collected to isolate the peripheral blood mononuclear cells, and to further obtain the NK cells after culture. NK cell suspension was intraperitoneally perfused into the abdominal cavity (no less than 2×109 cells/ time). The volume of peritoneal effusion, the level of serum tumor marker CA-125, the level of serum cytokines IL-2, INF-γ and TNF-α as well as the changes in peripheral blood lymphocyte subsets were detected before and after the treatment; Moreover, the clinical efficacy and adverse reactions were observed. Results: The effective rate of intraperitoneal perfusion of NK cells was 66.7%, and there were no obvious treatment-related adverse reactions. Compared with before treatment, the serum tumor marker CA-125 level significantly decreased after treatment (P<0.05), and the levels of IL-15, IFN-γ and TNF-α increased significantly (P<0.05 or P<0.01), while there was no significant changes in peripheral blood lymphocyte subsets (all P>0.05). Conclusion: Intraperitoneal infusion of NK cells in the treatment of ovarian cancer associated peritoneal effusion has a good short-term clinical efficacy with little adverse reactions, which is a promising method for the treatment of cancerous peritoneal effusion.
Objective: To investigate the short-term clinical efficacy and safety of intraperitoneal perfusion of natural killer (NK) cells in the treatment of ovarian cancer with ascites. Methods: The clinical data of 15 ovarian cancer patients with ascites effusion, who received NK cell perfusion in the Qinhuai Medical District of the General Hospital of Eastern Theater Command from November 2016 to January 2019, were analyzed. The peripheral blood was collected to isolate the peripheral blood mononuclear cells, and to further obtain the NK cells after culture. NK cell suspension was intraperitoneally perfused into the abdominal cavity (no less than 2×109 cells/ time). The volume of peritoneal effusion, the level of serum tumor marker CA-125, the level of serum cytokines IL-2, INF-γ and TNF-α as well as the changes in peripheral blood lymphocyte subsets were detected before and after the treatment; Moreover, the clinical efficacy and adverse reactions were observed. Results: The effective rate of intraperitoneal perfusion of NK cells was 66.7%, and there were no obvious treatment-related adverse reactions. Compared with before treatment, the serum tumor marker CA-125 level significantly decreased after treatment (P<0.05), and the levels of IL-15, IFN-γ and TNF-α increased significantly (P<0.05 or P<0.01), while there was no significant changes in peripheral blood lymphocyte subsets (all P>0.05). Conclusion: Intraperitoneal infusion of NK cells in the treatment of ovarian cancer associated peritoneal effusion has a good short-term clinical efficacy with little adverse reactions, which is a promising method for the treatment of cancerous peritoneal effusion.
2020, 27(10):1156-1161.
DOI: 10.3872/j.issn.1007-385X.2020.10.014
Abstract:
作为一种常见的非黑色素瘤皮肤癌，晚期皮肤鳞状细胞癌（cutaneous squamous cell carcinoma，cSCC）的治疗仍是急需 解决的临床难题。尽管cSCC并非靶向治疗研究的重点，但近年来随着靶向治疗在其他肿瘤的研究和应用的深入，cSCC的靶向 治疗也取得新的进展，特别是针对PD-1的免疫检查点疗法已经获准进入临床应用；针对另一些靶点如细胞表皮生长因子受体 （EGFR）、血管内皮生长因子受体（VEGFR）、胰岛素样生长因子受体（IGFR）以及肿瘤抗原MAGE-A3等的疗法也正在临床试用； TP53、CDKN2A和Notch等cSCC频繁突变的基因，以及RAS-RAF-MEK-ERK与PI3K-AKT-mTOR等通路相关信号分子和端粒酶 等也是具有研发潜力的cSCC治疗靶点，针对这些靶点开展深入研究有可能为cSCC的治疗找到新的途径。
作为一种常见的非黑色素瘤皮肤癌，晚期皮肤鳞状细胞癌（cutaneous squamous cell carcinoma，cSCC）的治疗仍是急需 解决的临床难题。尽管cSCC并非靶向治疗研究的重点，但近年来随着靶向治疗在其他肿瘤的研究和应用的深入，cSCC的靶向 治疗也取得新的进展，特别是针对PD-1的免疫检查点疗法已经获准进入临床应用；针对另一些靶点如细胞表皮生长因子受体 （EGFR）、血管内皮生长因子受体（VEGFR）、胰岛素样生长因子受体（IGFR）以及肿瘤抗原MAGE-A3等的疗法也正在临床试用； TP53、CDKN2A和Notch等cSCC频繁突变的基因，以及RAS-RAF-MEK-ERK与PI3K-AKT-mTOR等通路相关信号分子和端粒酶 等也是具有研发潜力的cSCC治疗靶点，针对这些靶点开展深入研究有可能为cSCC的治疗找到新的途径。
2020, 27(10):1162-1169.
DOI: 10.3872/j.issn.1007-385X.2020.10.015
Abstract:
DDX解旋酶（DEAD-box RNAhelicases）是经典的ATP依赖性解旋酶家族，目前已知共有50多个家族成员，主要发挥 RNA加工代谢相关调控作用，尤其是经典的RNA解旋功能被学界公认为DDX解旋酶最基本的功能。近年来，DDX解旋酶家族 成员已被发现与亚细胞结构动态转换、细胞周期转换、抗病毒免疫应答、胚胎形成、机体精子发生、能量物质代谢等生理过程密切 相关，而目前更为关注的是其在肿瘤发生发展病理过程中所发挥的重要作用，且部分DDX家族分子已经成为肿瘤诊断、预后评 估以及药物治疗的潜在靶点，为未来的临床治疗决策注入强大的活力。本文主要针对DDX家族分子的结构、生物学功能、营养 物质代谢、天然免疫及肿瘤发生与治疗等方面的研究展开综述。
DDX解旋酶（DEAD-box RNAhelicases）是经典的ATP依赖性解旋酶家族，目前已知共有50多个家族成员，主要发挥 RNA加工代谢相关调控作用，尤其是经典的RNA解旋功能被学界公认为DDX解旋酶最基本的功能。近年来，DDX解旋酶家族 成员已被发现与亚细胞结构动态转换、细胞周期转换、抗病毒免疫应答、胚胎形成、机体精子发生、能量物质代谢等生理过程密切 相关，而目前更为关注的是其在肿瘤发生发展病理过程中所发挥的重要作用，且部分DDX家族分子已经成为肿瘤诊断、预后评 估以及药物治疗的潜在靶点，为未来的临床治疗决策注入强大的活力。本文主要针对DDX家族分子的结构、生物学功能、营养 物质代谢、天然免疫及肿瘤发生与治疗等方面的研究展开综述。
2020, 27(10):1170-1176.
DOI: 10.3872/j.issn.1007-385X.2020.10.016
Abstract:
固有免疫和适应性免疫系统的免疫细胞组成肿瘤微环境（tumor microenvironment，TME），IL-1家族成员是TME中细 胞之间相互作用的主要介质，在多种微生物识别途径的交叉路口，具有激活和定位淋巴细胞的功能。IL-1家族成员是固有免疫 和适应性免疫的关键调节因子，这些细胞因子的作用根据所涉及的组织和器官，炎性背景和肿瘤的阶段而有很大不同，其促肿瘤 或抗肿瘤作用根据这些细胞因子由浸润肿瘤的免疫群体还是由肿瘤细胞产生所决定。肿瘤有能力形成其免疫微环境，以抵消宿 主免疫系统的消灭，肿瘤免疫治疗的一个关键挑战是克服肿瘤引起的免疫抑制。本文就近年来IL-1家族的生物学功能及其在肿 瘤免疫治疗方面的研究进展作一综述，以期为肿瘤的免疫治疗提供新思路。
固有免疫和适应性免疫系统的免疫细胞组成肿瘤微环境（tumor microenvironment，TME），IL-1家族成员是TME中细 胞之间相互作用的主要介质，在多种微生物识别途径的交叉路口，具有激活和定位淋巴细胞的功能。IL-1家族成员是固有免疫 和适应性免疫的关键调节因子，这些细胞因子的作用根据所涉及的组织和器官，炎性背景和肿瘤的阶段而有很大不同，其促肿瘤 或抗肿瘤作用根据这些细胞因子由浸润肿瘤的免疫群体还是由肿瘤细胞产生所决定。肿瘤有能力形成其免疫微环境，以抵消宿 主免疫系统的消灭，肿瘤免疫治疗的一个关键挑战是克服肿瘤引起的免疫抑制。本文就近年来IL-1家族的生物学功能及其在肿 瘤免疫治疗方面的研究进展作一综述，以期为肿瘤的免疫治疗提供新思路。
2020, 27(10):1177-1182.
DOI: 10.3872/j.issn.1007-385X.2020.10.017
Abstract:
循环肿瘤细胞（circulating tumor cell，CTC）是从原发肿瘤分离进入外周血或淋巴循环的肿瘤细胞，与肿瘤转移密切相 关。CTC作为液体活检重要标志物之一，支持实时动态重复检测，对于肿瘤的早期筛查、转移抑制、预后评估、复发监测、个性化 治疗指导具有重要意义。然而CTC在血液中含量极低，寻找稳定性好、灵敏度高及特异性强的CTC检测方法是当前研究的热 点。近年来，磁性纳米载体由于生物相容性好、表面易修饰和磁响应速度快等优势在CTC检测中受到广泛关注。本文阐述了 CTC检测的意义，系统归纳了磁性纳米载体用于CTC检测的设计方案，通过巧妙设计构建理想的磁性纳米载体，包括CTC的特 异性捕获，在特定刺激下实现CTC的释放，并对其捕获与释放过程进行监测，从而实现CTC的高效检测。
循环肿瘤细胞（circulating tumor cell，CTC）是从原发肿瘤分离进入外周血或淋巴循环的肿瘤细胞，与肿瘤转移密切相 关。CTC作为液体活检重要标志物之一，支持实时动态重复检测，对于肿瘤的早期筛查、转移抑制、预后评估、复发监测、个性化 治疗指导具有重要意义。然而CTC在血液中含量极低，寻找稳定性好、灵敏度高及特异性强的CTC检测方法是当前研究的热 点。近年来，磁性纳米载体由于生物相容性好、表面易修饰和磁响应速度快等优势在CTC检测中受到广泛关注。本文阐述了 CTC检测的意义，系统归纳了磁性纳米载体用于CTC检测的设计方案，通过巧妙设计构建理想的磁性纳米载体，包括CTC的特 异性捕获，在特定刺激下实现CTC的释放，并对其捕获与释放过程进行监测，从而实现CTC的高效检测。
2020, 27(10):1183-1189.
DOI: 10.3872/j.issn.1007-385X.2020.10.018
Abstract:
近年来，表观遗传修饰在恶性肿瘤发生发展中的调控作用受到广泛关注。早期的表观遗传修饰研究主要集中于DNA 和蛋白质水平，随着RNA深度测序技术和生物信息学方法的发展， 以N6-甲基腺嘌呤（N6-methyladenosine, m6A）为主的RNA表 观遗传修饰逐渐成为生物科学领域的研究热点。m6A是存在于所有高等真核生物中最普遍的mRNA表观修饰，具有动态可逆的 特点，涉及许多复杂细胞过程的精细调控， 如RNA的加工、运输、定位、翻译及降解等。最新研究表明， m6A可通过“写入”、“擦 除”和“阅读”相关因子的异常表达，可逆地动态调节RNA运输、定位、翻译及降解等方面，通过多种机制在肿瘤的发生发展过程 中发挥促进或抑制作用。本文就近年来m6A的生物学特性、RNA修饰的调控机制及其在肿瘤发生发展中的作用研究进展作一综述。
近年来，表观遗传修饰在恶性肿瘤发生发展中的调控作用受到广泛关注。早期的表观遗传修饰研究主要集中于DNA 和蛋白质水平，随着RNA深度测序技术和生物信息学方法的发展， 以N6-甲基腺嘌呤（N6-methyladenosine, m6A）为主的RNA表 观遗传修饰逐渐成为生物科学领域的研究热点。m6A是存在于所有高等真核生物中最普遍的mRNA表观修饰，具有动态可逆的 特点，涉及许多复杂细胞过程的精细调控， 如RNA的加工、运输、定位、翻译及降解等。最新研究表明， m6A可通过“写入”、“擦 除”和“阅读”相关因子的异常表达，可逆地动态调节RNA运输、定位、翻译及降解等方面，通过多种机制在肿瘤的发生发展过程 中发挥促进或抑制作用。本文就近年来m6A的生物学特性、RNA修饰的调控机制及其在肿瘤发生发展中的作用研究进展作一综述。
2020, 27(10):1190-1192.
DOI: 10.3872/j.issn.1007-385X.2020.10.019
Abstract:
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- 《中国肿瘤生物治疗杂志》
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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.