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Volume 29,Issue 2,2022 Table of Contents
2022, 29(2):87-92.
DOI: 10.3872/j.issn.1007-385X.2022.02.001
Abstract:
Metabolic reprogramming is one of the characteristics of tumors and an important potential target for tumor therapy. The effect of the interaction between tumor and immune cells on metabolic reprogramming is one of the key factors determining the anti-tumor immune response. Tumor metabolism not only plays a key role in maintaining tumor genesis and survival, but also affects immune cells by releasing metabolites such as arginine and PGE2, thereby affecting the tumor immune microenvironment. The interaction between tumor cells and immune cells leads to metabolic competition in the tumor immune microenvironment, which limits the normal metabolism of nutrients and forms an acidic environment, and ultimately leads to a weakened anti-tumor immune response and the formation of an immunosuppressive microenvironment Moreover, there are alterations in metabolism of immune cells during the process of immune responses, that is metabolic reprogramming occurs in immune cells during their proliferation, differentiation and performance of cellular functions. Therefore, understanding the regulatory mechanism of metabolic reprogramming of tumor cells and immune cells in tumor immune microenvironment will enable researchers to find therapeutic means of targeting metabolic pathways in anti-tumor immunotherapy.
Metabolic reprogramming is one of the characteristics of tumors and an important potential target for tumor therapy. The effect of the interaction between tumor and immune cells on metabolic reprogramming is one of the key factors determining the anti-tumor immune response. Tumor metabolism not only plays a key role in maintaining tumor genesis and survival, but also affects immune cells by releasing metabolites such as arginine and PGE2, thereby affecting the tumor immune microenvironment. The interaction between tumor cells and immune cells leads to metabolic competition in the tumor immune microenvironment, which limits the normal metabolism of nutrients and forms an acidic environment, and ultimately leads to a weakened anti-tumor immune response and the formation of an immunosuppressive microenvironment Moreover, there are alterations in metabolism of immune cells during the process of immune responses, that is metabolic reprogramming occurs in immune cells during their proliferation, differentiation and performance of cellular functions. Therefore, understanding the regulatory mechanism of metabolic reprogramming of tumor cells and immune cells in tumor immune microenvironment will enable researchers to find therapeutic means of targeting metabolic pathways in anti-tumor immunotherapy.
2022, 29(2):93-100.
DOI: 10.3872/j.issn.1007-385X.2022.02.002
Abstract:
Objective: To investigate the expression of long non-coding RNA (lncRNA) small nucleolar RNA host gene 10 (SNHG10) in colorectal cancer tissues and cells and its effect on the invasion and migration of colorectal cancer cells and the underlying mechanism. Methods: From January 2018 to December 2019, 78 pairs of colorectal cancer tissue and para-cancerous tissues from the patients who had radical colorectal cancer resection in Henan Provincial People's Hospital were collected. Quantitative PCR (qPCR) was performed to quantify the levels of lncRNA SNHG10 and miR-532-3p in colorectal cancer tissues, colorectal cancer cell lines (SW480, SW620, HT-29 and LoVo) and human normal colorectal mucosal FHC cells; and their correlations with the clinicopathological features of colorectal cancer patients were further analyzed. Dual-luciferase reporter gene assay was used to validate the targeted relationship between lncRNA SNHG10 and miR-532-3p. After transfection with si-SNHG10 or miR-532-3p mimic or co-transfection of si-SNHG10 and miR-532-3p inhibitor, the invasion and migration of SW620 cells were detected by Transwell assay, and the protein expression of E-cadherin, N-cadherin and vimentin were detected by WB. Results: SNHG10 was highly expressed in colorectal cancer tissues and cells (all P<0.05), and its expression was related to TNM stage and distant metastasis (all P<0.05). miR-532-3p was lowly expressed in colorectal cancer tissues and cells, and its expression was correlated with TNM stage, lymphonode metastasis and distant metastasis (all P<0.05). The expression of SNHG10 and miR-532-3p in colorectal cancer tissues was negatively correlated (r=-0.225, P=0.048). Dual-luciferase reporter gene assay confirmed that SNHG10 targetedly regulated miR-532-3p. Both down-regulation of SNHG10 and up-regulation of miR-532-3p significantly inhibited the invasion and migration of SW620 cells (all P<0.05), up-regulated the expression of E-cadherin (P<0.05), while down-regulated the expression of N-cadherin and vimentin (all P<0.05). After transfection with miR-532-3p inhibitor, the inhibitory effect of knocking down the expression of lncRNA SNHG10 on the invasion and migration of colorectal cancer cells was reversed (all P<0.05). Conclusions: LncRNA SNHG10 is highly expressed in colorectal cancer and is associated with TNM stage and distant metastasis. LncRNA SNHG10 affects the invasion and metastasis of colorectal cancer cells by targeting miR-532-3p and regulating EMT.
Objective: To investigate the expression of long non-coding RNA (lncRNA) small nucleolar RNA host gene 10 (SNHG10) in colorectal cancer tissues and cells and its effect on the invasion and migration of colorectal cancer cells and the underlying mechanism. Methods: From January 2018 to December 2019, 78 pairs of colorectal cancer tissue and para-cancerous tissues from the patients who had radical colorectal cancer resection in Henan Provincial People's Hospital were collected. Quantitative PCR (qPCR) was performed to quantify the levels of lncRNA SNHG10 and miR-532-3p in colorectal cancer tissues, colorectal cancer cell lines (SW480, SW620, HT-29 and LoVo) and human normal colorectal mucosal FHC cells; and their correlations with the clinicopathological features of colorectal cancer patients were further analyzed. Dual-luciferase reporter gene assay was used to validate the targeted relationship between lncRNA SNHG10 and miR-532-3p. After transfection with si-SNHG10 or miR-532-3p mimic or co-transfection of si-SNHG10 and miR-532-3p inhibitor, the invasion and migration of SW620 cells were detected by Transwell assay, and the protein expression of E-cadherin, N-cadherin and vimentin were detected by WB. Results: SNHG10 was highly expressed in colorectal cancer tissues and cells (all P<0.05), and its expression was related to TNM stage and distant metastasis (all P<0.05). miR-532-3p was lowly expressed in colorectal cancer tissues and cells, and its expression was correlated with TNM stage, lymphonode metastasis and distant metastasis (all P<0.05). The expression of SNHG10 and miR-532-3p in colorectal cancer tissues was negatively correlated (r=-0.225, P=0.048). Dual-luciferase reporter gene assay confirmed that SNHG10 targetedly regulated miR-532-3p. Both down-regulation of SNHG10 and up-regulation of miR-532-3p significantly inhibited the invasion and migration of SW620 cells (all P<0.05), up-regulated the expression of E-cadherin (P<0.05), while down-regulated the expression of N-cadherin and vimentin (all P<0.05). After transfection with miR-532-3p inhibitor, the inhibitory effect of knocking down the expression of lncRNA SNHG10 on the invasion and migration of colorectal cancer cells was reversed (all P<0.05). Conclusions: LncRNA SNHG10 is highly expressed in colorectal cancer and is associated with TNM stage and distant metastasis. LncRNA SNHG10 affects the invasion and metastasis of colorectal cancer cells by targeting miR-532-3p and regulating EMT.
2022, 29(2):101-107.
DOI: 10.3872/j.issn.1007-385X.2022.02.003
Abstract:
Objective: To investigate the effects of fibronectin Ⅲ domain containing protein 10 (FNDC10) on the proliferation, migration and invasion of breast cancer cells, and to primarily explore the mechanism. Methods: TCGAdatabase was used to analyze the expression of FNDC10 in breast cancer tissues. The mRNAlevel of FNDC10 in normal immortalized breast cells (MCF-10A) and breast cancer cells (MCF-7, MDA-MB-231, BT549, MDA-MB-468, HCC1806, HCC1937) was detected by qPCR. MCF-7 and MDA-MB-231 cells were transfected with FNDC10 siRNA or NC-siRNA for functional experiments. CCK-8 assay was used to detect the effect of FNDC10 on the proliferation of breast cancer cells. Colony forming assay was used to detect the colony forming ability of breast cancer cells. Transwell assay was used to detect the effect of FNDC10 on migration and invasion of breast cancer cells. WB was used to detect the changes of metastasis- related molecules and cell signaling pathways at protein level. Results:The expression of FNDC10 in breast cancer tissues was significantly higher than that in normal tissues (P<0.01), and the expression level of FNDC10 in breast cancer MCF-7 and MDA-MB-231 cells was higher than that in normal breast cells (P<0.01 or P<0.05). Knocking down FNDC10 expression inhibited the proliferation, migration and invasion of breast cancer cells (P<0.01 or P<0.05). The mechanism study showed that knockdown of FNDC10 expression inhibited STAT3 activation in breast cancer cells (P<0.01 or P<0.05) and enhanced the expression of EMT maker E-cadherin (P<0.05), leading to the suppression of EMT progression. Conclusion: FNDC10 promotes proliferation and EMT of breast cancer cells through activating STAT3 signaling pathway, thereby promoting the malignant progression of breast cancer.
Objective: To investigate the effects of fibronectin Ⅲ domain containing protein 10 (FNDC10) on the proliferation, migration and invasion of breast cancer cells, and to primarily explore the mechanism. Methods: TCGAdatabase was used to analyze the expression of FNDC10 in breast cancer tissues. The mRNAlevel of FNDC10 in normal immortalized breast cells (MCF-10A) and breast cancer cells (MCF-7, MDA-MB-231, BT549, MDA-MB-468, HCC1806, HCC1937) was detected by qPCR. MCF-7 and MDA-MB-231 cells were transfected with FNDC10 siRNA or NC-siRNA for functional experiments. CCK-8 assay was used to detect the effect of FNDC10 on the proliferation of breast cancer cells. Colony forming assay was used to detect the colony forming ability of breast cancer cells. Transwell assay was used to detect the effect of FNDC10 on migration and invasion of breast cancer cells. WB was used to detect the changes of metastasis- related molecules and cell signaling pathways at protein level. Results:The expression of FNDC10 in breast cancer tissues was significantly higher than that in normal tissues (P<0.01), and the expression level of FNDC10 in breast cancer MCF-7 and MDA-MB-231 cells was higher than that in normal breast cells (P<0.01 or P<0.05). Knocking down FNDC10 expression inhibited the proliferation, migration and invasion of breast cancer cells (P<0.01 or P<0.05). The mechanism study showed that knockdown of FNDC10 expression inhibited STAT3 activation in breast cancer cells (P<0.01 or P<0.05) and enhanced the expression of EMT maker E-cadherin (P<0.05), leading to the suppression of EMT progression. Conclusion: FNDC10 promotes proliferation and EMT of breast cancer cells through activating STAT3 signaling pathway, thereby promoting the malignant progression of breast cancer.
2022, 29(2):108-113.
DOI: 10.3872/j.issn.1007-385X.2022.02.004
Abstract:
Objective: To investigate the effect of lncRNA SNHG11 on the proliferation, invasion and migration of non-small cell lung cancer (NSCLC) A549 cells and its possible mechanisms. Methods: qPCR was used to detect the levels of lncRNA SNHG11 and miR- 193a-5p in human embryonic lung cells (HEL-1) and lung cancer cells (A549, H1299, and HCC827). A549 cells were transfected with SNHG11 small interfering RNA (si-SNHG11), miR-193a mimic or miR-193a inhibitor. The proliferation of A549 cells was detected by CCK-8 assay, migration and invasion of A549 cells were detected by Wound healing and Transwell assay, the protein expression of Ki67 and Cyclin D1 was determined by Western blot, and the targeting relationship between lncRNA SNHG11 and miR-193a-5p was verified by Dual-luciferase reporter experiment. Results: Compared with HEL-1 cells, the expression level of lncRNA SNHG11 was significantly increased while the expression of miR-193a-5p was decreased in lung cancer A549, H1299 and HCC827 cells (all P<0.05). Silencing lncRNA SNHG11 inhibited the proliferation, migration and invasion of A549 cells and reduced the protein expression of Ki67 and Cyclin D1 (all P<0.05). Over-expression of miR-193a-5p inhibited the proliferation, migration and invasion of A549 cells (all P<0.05). lncRNA SNHG11 could targetedly adsorb miR-193a-5p. miR-139a-5p inhibition could partially reverse the effect of silencing lncRNA SNHG11 on the proliferation, invasion and migration of A549 cells (all P<0.05). Conclusion: lncRNA SNHG11 promotes the proliferation, invasion and migration of NSCLC cells by adsorbing miR-193a-5p.
Objective: To investigate the effect of lncRNA SNHG11 on the proliferation, invasion and migration of non-small cell lung cancer (NSCLC) A549 cells and its possible mechanisms. Methods: qPCR was used to detect the levels of lncRNA SNHG11 and miR- 193a-5p in human embryonic lung cells (HEL-1) and lung cancer cells (A549, H1299, and HCC827). A549 cells were transfected with SNHG11 small interfering RNA (si-SNHG11), miR-193a mimic or miR-193a inhibitor. The proliferation of A549 cells was detected by CCK-8 assay, migration and invasion of A549 cells were detected by Wound healing and Transwell assay, the protein expression of Ki67 and Cyclin D1 was determined by Western blot, and the targeting relationship between lncRNA SNHG11 and miR-193a-5p was verified by Dual-luciferase reporter experiment. Results: Compared with HEL-1 cells, the expression level of lncRNA SNHG11 was significantly increased while the expression of miR-193a-5p was decreased in lung cancer A549, H1299 and HCC827 cells (all P<0.05). Silencing lncRNA SNHG11 inhibited the proliferation, migration and invasion of A549 cells and reduced the protein expression of Ki67 and Cyclin D1 (all P<0.05). Over-expression of miR-193a-5p inhibited the proliferation, migration and invasion of A549 cells (all P<0.05). lncRNA SNHG11 could targetedly adsorb miR-193a-5p. miR-139a-5p inhibition could partially reverse the effect of silencing lncRNA SNHG11 on the proliferation, invasion and migration of A549 cells (all P<0.05). Conclusion: lncRNA SNHG11 promotes the proliferation, invasion and migration of NSCLC cells by adsorbing miR-193a-5p.
2022, 29(2):114-119.
DOI: 10.3872/j.issn.1007-385X.2022.02.005
Abstract:
Objective: To analyze the expression of miR-185 and cell division cyclin 42 (CDC42) in osteosarcoma tissues and cells, and to preliminarily explore whether miR-185 affects the proliferation and migration of osteosarcoma MG63 cells by regulating CDC42. Methods: The cancer tissues and para-cancerous tissues of 28 patients with osteosarcoma that pathologically confirmed in the Fourth People's Hospital of Hengshui City from January 2020 to January 2021 were collected for this study. Immunohistochemistry was used to detect the expression of CDC42 in osteosarcoma tissues, and qPCR was used to detect the expression of miR-185 in osteosarcoma tissues. Dual-luciferase reporter gene experiment was applied to verify the targeting relationship between CDC42 and miR-185. According to different transfectants, MG63 cells were divided into miR-185 mimic group, miR-NC group, miR-185 inhibitor group, NC-inhibitor group, CDC42 group (transfected with CDC42 over-expression vector), and negative control (NC) group. The effects of miR-185 and CDC42 expression on the migration, proliferation and cell cycle of MG63 cells were detected by scratch healing assay, CCK-8 method and FCM, respectively. A nude mouse xenograft model was constructed by inoculating osteosarcoma MG63 cells. Immunohistochemistry, qPCR and WB methods were used to detect the effects of over-expression or knock-down of miR-185 on the expression of Ki67 and CDC42 in transplanted tumor tissues. Results: Compared with para-cancerous tissues, the expression of miR-185 in osteosarcoma tissues was significantly decreased, while the expression of CDC42 was significantly increased (all P<0.01). CDC42 was verified to be a target gene of miR-185. Compared with the control group, the migration and proliferation of MG63 cells in the miR-185 mimic group were inhibited (all P<0.01), while the migration and proliferation of MG63 cells in the CDC42 group were increased and the cell cycle was arrested in the S phase (all P<0.01). Compared with the miR-185 group, the migration and proliferation abilities of MG63 cells in the miR-185+CDC42 group were promoted, and the proportion of cells in S phase was increased (all P<0.01). Compared with the control group, the expression of Ki67 and CDC42 in the transplanted tumor tissues of miR-185 mimic group was significantly decreased (all P<0.01), while the opposite results were observed in miR-185 inhibitor group (all P<0.01). Conclusion: miR-185 is lowly expressed while CDC42 is highly expressed in osteosarcoma tissues. miR-185 can inhibit the proliferation and migration of osteosarcoma MG63 cells by negatively regulating the expression of CDC42.
Objective: To analyze the expression of miR-185 and cell division cyclin 42 (CDC42) in osteosarcoma tissues and cells, and to preliminarily explore whether miR-185 affects the proliferation and migration of osteosarcoma MG63 cells by regulating CDC42. Methods: The cancer tissues and para-cancerous tissues of 28 patients with osteosarcoma that pathologically confirmed in the Fourth People's Hospital of Hengshui City from January 2020 to January 2021 were collected for this study. Immunohistochemistry was used to detect the expression of CDC42 in osteosarcoma tissues, and qPCR was used to detect the expression of miR-185 in osteosarcoma tissues. Dual-luciferase reporter gene experiment was applied to verify the targeting relationship between CDC42 and miR-185. According to different transfectants, MG63 cells were divided into miR-185 mimic group, miR-NC group, miR-185 inhibitor group, NC-inhibitor group, CDC42 group (transfected with CDC42 over-expression vector), and negative control (NC) group. The effects of miR-185 and CDC42 expression on the migration, proliferation and cell cycle of MG63 cells were detected by scratch healing assay, CCK-8 method and FCM, respectively. A nude mouse xenograft model was constructed by inoculating osteosarcoma MG63 cells. Immunohistochemistry, qPCR and WB methods were used to detect the effects of over-expression or knock-down of miR-185 on the expression of Ki67 and CDC42 in transplanted tumor tissues. Results: Compared with para-cancerous tissues, the expression of miR-185 in osteosarcoma tissues was significantly decreased, while the expression of CDC42 was significantly increased (all P<0.01). CDC42 was verified to be a target gene of miR-185. Compared with the control group, the migration and proliferation of MG63 cells in the miR-185 mimic group were inhibited (all P<0.01), while the migration and proliferation of MG63 cells in the CDC42 group were increased and the cell cycle was arrested in the S phase (all P<0.01). Compared with the miR-185 group, the migration and proliferation abilities of MG63 cells in the miR-185+CDC42 group were promoted, and the proportion of cells in S phase was increased (all P<0.01). Compared with the control group, the expression of Ki67 and CDC42 in the transplanted tumor tissues of miR-185 mimic group was significantly decreased (all P<0.01), while the opposite results were observed in miR-185 inhibitor group (all P<0.01). Conclusion: miR-185 is lowly expressed while CDC42 is highly expressed in osteosarcoma tissues. miR-185 can inhibit the proliferation and migration of osteosarcoma MG63 cells by negatively regulating the expression of CDC42.
2022, 29(2):120-127.
DOI: 10.3872/j.issn.1007-385X.2022.02.006
Abstract:
Objective: To investigate the expression of tight junction protein claudin-7 (CLDN-7) in pancreatic cancer and its correlation with the clinicopathological features and prognosis of pancreatic cancer patients. Methods: Oncomine, GEPIA and GEO databases were used to comprehensively analyze the mRNA expression level of CLDN-7 in pancreatic cancer, and Kaplan-Meier Plotter database was used to analyze the relationship between the expression of CLDN-7 and the survival prognosis of pancreatic cancer patients. Immunohistochemical staining was used to detect the protein level of CLDN-7 in 44 cases of pancreatic cancer tissues and 31 cases of para-cancerous tissues resected in the Department of General Surgery of the Second Hospital of Lanzhou University from 2015 to 2018, and the relationship between CLDN-7 expression and clinicopathological characteristics and prognosis of patients was also analyzed. GO (Gene Ontology) analysis and KEGG (Kyoto Encyclopedia of Genes and Genomes) pathway enrichment analysis were conducted to analyze the possible signaling pathways that CLDN-7 may involve in and their main functions, which were further verified in TCGA and GEPIA databases. Results: Analysis of both the databases and the clinical samples showed that CLDN-7 was significantly over-expressed in pancreatic cancer tissues, and its high expression was correlated with clinical prognosis of pancreatic cancer patients; moreover, CLDN-7 expression was an independent factor affecting the overall survival time of pancreatic cancer patients (all P<0.05). GO analysis and KEGG pathway enrichment analysis confirmed that CLDN-7 was involved in DNA damage repair and glucose metabolism in pancreatic cancer patients. TCGA and GEPIA database validation showed that CLDN-7 expression in pancreatic cancer was significantly and positively correlated with the expression of DNA damage repair related genes (POLD4, SMUG1, NTHL1) and glucose metabolism related genes (ALDOA, TALDO1, PGLS) (all P<0.01). Conclusion: CLDN-7 is highly expressed in pancreatic cancer and indicates a worse clinical prognosis; moreover, CLDN-7 is associated with DNA damage repair and intratumoral glucose metabolism in pancreatic cancer.
Objective: To investigate the expression of tight junction protein claudin-7 (CLDN-7) in pancreatic cancer and its correlation with the clinicopathological features and prognosis of pancreatic cancer patients. Methods: Oncomine, GEPIA and GEO databases were used to comprehensively analyze the mRNA expression level of CLDN-7 in pancreatic cancer, and Kaplan-Meier Plotter database was used to analyze the relationship between the expression of CLDN-7 and the survival prognosis of pancreatic cancer patients. Immunohistochemical staining was used to detect the protein level of CLDN-7 in 44 cases of pancreatic cancer tissues and 31 cases of para-cancerous tissues resected in the Department of General Surgery of the Second Hospital of Lanzhou University from 2015 to 2018, and the relationship between CLDN-7 expression and clinicopathological characteristics and prognosis of patients was also analyzed. GO (Gene Ontology) analysis and KEGG (Kyoto Encyclopedia of Genes and Genomes) pathway enrichment analysis were conducted to analyze the possible signaling pathways that CLDN-7 may involve in and their main functions, which were further verified in TCGA and GEPIA databases. Results: Analysis of both the databases and the clinical samples showed that CLDN-7 was significantly over-expressed in pancreatic cancer tissues, and its high expression was correlated with clinical prognosis of pancreatic cancer patients; moreover, CLDN-7 expression was an independent factor affecting the overall survival time of pancreatic cancer patients (all P<0.05). GO analysis and KEGG pathway enrichment analysis confirmed that CLDN-7 was involved in DNA damage repair and glucose metabolism in pancreatic cancer patients. TCGA and GEPIA database validation showed that CLDN-7 expression in pancreatic cancer was significantly and positively correlated with the expression of DNA damage repair related genes (POLD4, SMUG1, NTHL1) and glucose metabolism related genes (ALDOA, TALDO1, PGLS) (all P<0.01). Conclusion: CLDN-7 is highly expressed in pancreatic cancer and indicates a worse clinical prognosis; moreover, CLDN-7 is associated with DNA damage repair and intratumoral glucose metabolism in pancreatic cancer.
2022, 29(2):128-134.
DOI: 10.3872/j.issn.1007-385X.2022.02.007
Abstract:
Objective: To investigate the effect of circAGFG1 on the proliferation, migration and invasion of cholangiocarcinoma QBC939 cells and its possible mechanism. Methods: The tumor tissues and corresponding para-cancerous tissues of 33 patients with cholangiocarcinoma who underwent surgical resection in the 988th Hospital of the Joint Logistics Support Force from April 2017 to October 2019 were collected. qPCR was used to detect the expression level of circAGFG1 and miR-4429 in the tissues. Cholangiocarcinoma QBC939 cells were cultured in vitro and transfected with si-circAGFG1 or miR-4429 mimics, or co-transfected with si-circAGFG1 and anti-miR-4429. Then, cell proliferation was detected by CCK-8 method and clone formation test, cell migration and invasion were detected by scratch test and Transwell assay, and the protein expression of E-cadherin and N-cadherin in cells was determined by Western blotting. Dual-luciferase reporter gene experiment was adopted to verify the regulatory relationship between circAGFG1 and miR-4429. Results: The expression of circAGFG1 was higher (3.89±0.26 vs 1.00±0.08, P<0.05) while the expression of miR-4429 (0.28±0.03 vs 1.00±0.05, P<0.05) was lower in cholangiocarcinoma tissues than those in para-cancerous tissues. After the interference with circAGFG1 or over-expression of miR-4429, the cell proliferation level, number of clone formation, scratch healing rate, number of invaded cells, and the protein expression of N-cadherin in QBC939 cells were reduced (all P<0.05), but the protein expression of E-cadherin was elevated (P<0.05). circAGFG1 could targetedly bind with miR-4429, and interfering circAGFG1 promoted the expression of miR-4429 in QBC939 cells (all P<0.05). Down-regulation of miR-4429 reversed the effect of interfering circAGFG1 on the proliferation, migration and invasion of QBC939 cells (all P<0.05). Conclusion: The expression of circAGFG1 is up-regulated in cholangiocarcinoma tissues, which may promote the proliferation, migration and invasion of cholangiocarcinoma QBC939 cells by targetedly inhibiting the expression of miR-4429.
Objective: To investigate the effect of circAGFG1 on the proliferation, migration and invasion of cholangiocarcinoma QBC939 cells and its possible mechanism. Methods: The tumor tissues and corresponding para-cancerous tissues of 33 patients with cholangiocarcinoma who underwent surgical resection in the 988th Hospital of the Joint Logistics Support Force from April 2017 to October 2019 were collected. qPCR was used to detect the expression level of circAGFG1 and miR-4429 in the tissues. Cholangiocarcinoma QBC939 cells were cultured in vitro and transfected with si-circAGFG1 or miR-4429 mimics, or co-transfected with si-circAGFG1 and anti-miR-4429. Then, cell proliferation was detected by CCK-8 method and clone formation test, cell migration and invasion were detected by scratch test and Transwell assay, and the protein expression of E-cadherin and N-cadherin in cells was determined by Western blotting. Dual-luciferase reporter gene experiment was adopted to verify the regulatory relationship between circAGFG1 and miR-4429. Results: The expression of circAGFG1 was higher (3.89±0.26 vs 1.00±0.08, P<0.05) while the expression of miR-4429 (0.28±0.03 vs 1.00±0.05, P<0.05) was lower in cholangiocarcinoma tissues than those in para-cancerous tissues. After the interference with circAGFG1 or over-expression of miR-4429, the cell proliferation level, number of clone formation, scratch healing rate, number of invaded cells, and the protein expression of N-cadherin in QBC939 cells were reduced (all P<0.05), but the protein expression of E-cadherin was elevated (P<0.05). circAGFG1 could targetedly bind with miR-4429, and interfering circAGFG1 promoted the expression of miR-4429 in QBC939 cells (all P<0.05). Down-regulation of miR-4429 reversed the effect of interfering circAGFG1 on the proliferation, migration and invasion of QBC939 cells (all P<0.05). Conclusion: The expression of circAGFG1 is up-regulated in cholangiocarcinoma tissues, which may promote the proliferation, migration and invasion of cholangiocarcinoma QBC939 cells by targetedly inhibiting the expression of miR-4429.
2022, 29(2):135-141.
DOI: 10.3872/j.issn.1007-385X.2022.02.008
Abstract:
三阴乳腺癌作为乳腺癌的一种独立临床病理类型，具有总生存期短、恶性程度高、侵袭能力强及早期复发率高等特点，目前治疗仍以化疗为主。新抗原是由体细胞DNA突变产生的肿瘤特异性抗原，在免疫治疗中与疗效和预后具有一定的相关性，肿瘤新抗原的研究有望进一步揭示免疫治疗的机制，近年来已经成为肿瘤领域研究热点。本文综述了肿瘤新抗原的鉴定识别、新抗原与免疫治疗的关系、新抗原疫苗及在三阴性乳腺癌中的相关进展。
三阴乳腺癌作为乳腺癌的一种独立临床病理类型，具有总生存期短、恶性程度高、侵袭能力强及早期复发率高等特点，目前治疗仍以化疗为主。新抗原是由体细胞DNA突变产生的肿瘤特异性抗原，在免疫治疗中与疗效和预后具有一定的相关性，肿瘤新抗原的研究有望进一步揭示免疫治疗的机制，近年来已经成为肿瘤领域研究热点。本文综述了肿瘤新抗原的鉴定识别、新抗原与免疫治疗的关系、新抗原疫苗及在三阴性乳腺癌中的相关进展。
2022, 29(2):142-149.
DOI: 10.3872/j.issn.1007-385X.2022.02.009
Abstract:
肿瘤免疫研究新平台 — — 肿瘤组织微环境类器官，因其保留了体内肿瘤微环境（TME）的特征，在肿瘤免疫治疗领域的应用有明显的优势。根据是否需要添加外源免疫细胞以及基质细胞可以将模拟TME的类器官模型分为初始TME类器官培养模型（native TME model）和重建TME类器官培养模型（reconstituted TME model）两种。介绍两种模型的体外培养方法和其在肿瘤免疫治疗临床前研究中的应用，如鉴定生物标志物、评估免疫联合治疗策略的疗效、制备肿瘤特异性T细胞和筛选免疫治疗新方法等，并对该平台目前存在的短板和局限性以及未来的发展前景等进行初步分析和展望，以期为该领域研究提供参考和帮助。
肿瘤免疫研究新平台 — — 肿瘤组织微环境类器官，因其保留了体内肿瘤微环境（TME）的特征，在肿瘤免疫治疗领域的应用有明显的优势。根据是否需要添加外源免疫细胞以及基质细胞可以将模拟TME的类器官模型分为初始TME类器官培养模型（native TME model）和重建TME类器官培养模型（reconstituted TME model）两种。介绍两种模型的体外培养方法和其在肿瘤免疫治疗临床前研究中的应用，如鉴定生物标志物、评估免疫联合治疗策略的疗效、制备肿瘤特异性T细胞和筛选免疫治疗新方法等，并对该平台目前存在的短板和局限性以及未来的发展前景等进行初步分析和展望，以期为该领域研究提供参考和帮助。
2022, 29(2):150-156.
DOI: 10.3872/j.issn.1007-385X.2022.02.010
Abstract:
目前，针对抑制性受体或配体、PD-1/PD-L1及CTLA-4的靶向免疫治疗已经取得了显著的临床成果，然而仍有许多患者未从免疫治疗中获益。因此，有必要寻找新的靶点及治疗方法，以提高免疫治疗的应答率。淋巴细胞上的T细胞免疫球蛋白及其ITIM结构域（T-cell immunoreceptor with immunoglobulin and ITIM domains，TIGIT）、CD226和CD112R等均属于免疫球蛋白超家族受体，与不同配体结合后传递抑制或激活信号，他们复杂的相互作用形成的整合信号能够调节免疫细胞的功能。对靶向TIGIT、CD226和CD112R的免疫治疗研究进展进行综述，包括TIGIT、CD226、CD112R的生物学特性，抑制肿瘤或促进肿瘤的机制，靶向治疗的研究进展。
目前，针对抑制性受体或配体、PD-1/PD-L1及CTLA-4的靶向免疫治疗已经取得了显著的临床成果，然而仍有许多患者未从免疫治疗中获益。因此，有必要寻找新的靶点及治疗方法，以提高免疫治疗的应答率。淋巴细胞上的T细胞免疫球蛋白及其ITIM结构域（T-cell immunoreceptor with immunoglobulin and ITIM domains，TIGIT）、CD226和CD112R等均属于免疫球蛋白超家族受体，与不同配体结合后传递抑制或激活信号，他们复杂的相互作用形成的整合信号能够调节免疫细胞的功能。对靶向TIGIT、CD226和CD112R的免疫治疗研究进展进行综述，包括TIGIT、CD226、CD112R的生物学特性，抑制肿瘤或促进肿瘤的机制，靶向治疗的研究进展。
2022, 29(2):157-162.
DOI: 10.3872/j.issn.1007-385X.2022.02.011
Abstract:
IFN-γ在抗肿瘤过程中发挥了重要作用，近年来人们逐渐认识到了其在肿瘤免疫治疗中的必要性。IFN-γ作用于肿瘤发生发展的全过程，其在抗肿瘤方面的作用机制主要分为免疫机制和非免疫机制。IFN-γ可以直接抑制肿瘤细胞增殖、促进肿瘤细胞凋亡、抑制肿瘤血管生成，协同固有免疫和适应性免疫的NK、NKT细胞、γδT细胞以及CD4 + /CD8 + T细胞等完成肿瘤杀伤。然而也有报道IFN-γ的促肿瘤作用，主要表现为在长期慢性炎症和肿瘤微环境中重塑免疫微环境促进免疫逃逸。因此，在肿瘤免疫治疗中要注意IFN-γ的双向效应，防止产生定向选择造成肿瘤免疫抑制。
IFN-γ在抗肿瘤过程中发挥了重要作用，近年来人们逐渐认识到了其在肿瘤免疫治疗中的必要性。IFN-γ作用于肿瘤发生发展的全过程，其在抗肿瘤方面的作用机制主要分为免疫机制和非免疫机制。IFN-γ可以直接抑制肿瘤细胞增殖、促进肿瘤细胞凋亡、抑制肿瘤血管生成，协同固有免疫和适应性免疫的NK、NKT细胞、γδT细胞以及CD4 + /CD8 + T细胞等完成肿瘤杀伤。然而也有报道IFN-γ的促肿瘤作用，主要表现为在长期慢性炎症和肿瘤微环境中重塑免疫微环境促进免疫逃逸。因此，在肿瘤免疫治疗中要注意IFN-γ的双向效应，防止产生定向选择造成肿瘤免疫抑制。
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- 《中国肿瘤生物治疗杂志》
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Chinese Journal Of Cancer Biotheray ® 2025 All Rights Reserved
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Chinese Journal Of Cancer Biotheray ® 2025 All Rights Reserved
Supported by:Beijing E-Tiller Technology Development Co., Ltd.