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Volume 31,Issue 3,2024 Table of Contents
2024, 31(3):211-218.
DOI: 10.3872/j.issn.1007-385X.2024.03.001
Abstract:
γδT cell is a unique kind of innate immune T cell expressing T cell receptor γ and δ chain heterodimer. There is a lack of comprehensive and systematic basic research in the development, differentiation, proliferation, activation, effect and exhaustion of γδT cell that many main questions are remaining unclear. However, mature γδT cells predominantly colonize mucosal tissues with a high incidence of tumors, such as skin, digestive tract, respiratory tract, and reproductive tract, and can directly recognize and kill a variety of tumor cells without major histocompatibility complex (MHC) restriction, which has irreplaceable advantages in the field of tumor immunotherapy. In recent years, the application of γδT cells have surged and developed rapidly, which, in turn, contributed to the deepening of basic research, and thus some brilliant progress has been made. In this paper, we enumerate the major progress of γδT cells in tumor immunotherapy in 2023, mainly focusing on the mechanism of tumor antigen recognition by γδT cells, the functional regulation of γδT cells in the tumor microenvironment, the mechanism of anti-tumor cytotoxicity of γδT cells, and the new synergistic strategy of tumor immunotherapy based on γδT cells. It is expected to promote the further development of γδT cells in the field of tumour immunotherapy and provide new insights into the synergistic strategy of γδT cells in clinical application.
γδT cell is a unique kind of innate immune T cell expressing T cell receptor γ and δ chain heterodimer. There is a lack of comprehensive and systematic basic research in the development, differentiation, proliferation, activation, effect and exhaustion of γδT cell that many main questions are remaining unclear. However, mature γδT cells predominantly colonize mucosal tissues with a high incidence of tumors, such as skin, digestive tract, respiratory tract, and reproductive tract, and can directly recognize and kill a variety of tumor cells without major histocompatibility complex (MHC) restriction, which has irreplaceable advantages in the field of tumor immunotherapy. In recent years, the application of γδT cells have surged and developed rapidly, which, in turn, contributed to the deepening of basic research, and thus some brilliant progress has been made. In this paper, we enumerate the major progress of γδT cells in tumor immunotherapy in 2023, mainly focusing on the mechanism of tumor antigen recognition by γδT cells, the functional regulation of γδT cells in the tumor microenvironment, the mechanism of anti-tumor cytotoxicity of γδT cells, and the new synergistic strategy of tumor immunotherapy based on γδT cells. It is expected to promote the further development of γδT cells in the field of tumour immunotherapy and provide new insights into the synergistic strategy of γδT cells in clinical application.
2024, 31(3):219-223.
DOI: 10.3872/j.issn.1007-385X.2024.03.002
Abstract:
Objective: To investigate the effects of resveratrol (Res) on the proliferation, invasion, and cell cycle of hepatobiliary carcinoma SMMC-7721 cells by regulating protein arginine methyltransferase 5 (PRMT5) expression and its underlying mechanism. Methods: Normal hepatocytes LO2 and hepatobiliary carcinoma SMMC-7721 cells were routinely cultured and treated with 20, 40, 80 μmol/L Res. qPCR assay was used to detect the mRNA expression of PRMT5 in LO2 cells, SMMC-7721 cells and Res-treated SMMC-7721 cells, respectively. The effects of Res on the proliferation, invasion, and cell cycle and apoptosis were examined using MTT assay, Transwell assay, and flow cytometry, respectively. WB assay was used to detect the protein expression of PRMT5, cyclin D1 and cyclin E1 in SMMC-7721 cells. Results: PRMT5 was highly expressed in SMMC-7721 cells (P<0.01). 20, 40, and 80 μmol/L Res significantly inhibited the mRNA and protein expression of PRMT5 in SMMC-7721 cells (all P<0.01), suppressed the proliferation (P<0.01) and invasion (P<0.05) abilities of SMMC-7721 cells, and blocked SMMC-7721 cell cycle in G2/M phase as well as promoted its apoptosis (all P<0.01); Besides, Res significantly inhibited the protein expression levels of cyclin D1 and cyclin E1 in SMMC-7721 cells (all P<0.01). Conclusion: PRMT5 is highly expressed in SMMC7721 cells. Res can effectively inhibit the proliferation and invasion abilities of SMMC-7721 cells and induce cell apoptosis, and its possible mechanism is related to the inhibition of PRMT5 expression.
Objective: To investigate the effects of resveratrol (Res) on the proliferation, invasion, and cell cycle of hepatobiliary carcinoma SMMC-7721 cells by regulating protein arginine methyltransferase 5 (PRMT5) expression and its underlying mechanism. Methods: Normal hepatocytes LO2 and hepatobiliary carcinoma SMMC-7721 cells were routinely cultured and treated with 20, 40, 80 μmol/L Res. qPCR assay was used to detect the mRNA expression of PRMT5 in LO2 cells, SMMC-7721 cells and Res-treated SMMC-7721 cells, respectively. The effects of Res on the proliferation, invasion, and cell cycle and apoptosis were examined using MTT assay, Transwell assay, and flow cytometry, respectively. WB assay was used to detect the protein expression of PRMT5, cyclin D1 and cyclin E1 in SMMC-7721 cells. Results: PRMT5 was highly expressed in SMMC-7721 cells (P<0.01). 20, 40, and 80 μmol/L Res significantly inhibited the mRNA and protein expression of PRMT5 in SMMC-7721 cells (all P<0.01), suppressed the proliferation (P<0.01) and invasion (P<0.05) abilities of SMMC-7721 cells, and blocked SMMC-7721 cell cycle in G2/M phase as well as promoted its apoptosis (all P<0.01); Besides, Res significantly inhibited the protein expression levels of cyclin D1 and cyclin E1 in SMMC-7721 cells (all P<0.01). Conclusion: PRMT5 is highly expressed in SMMC7721 cells. Res can effectively inhibit the proliferation and invasion abilities of SMMC-7721 cells and induce cell apoptosis, and its possible mechanism is related to the inhibition of PRMT5 expression.
2024, 31(3):224-230.
DOI: 10.3872/j.issn.1007-385X.2024.03.003
Abstract:
Objective: To investigate the effect of polydatin on malignant biological behaviors and cisplatin(DDP) -sensitivity of human thyroid cancer 8505C cells by regulating the Hippo/Yes-associated protein (YAP) signaling pathway. Methods: 8505C cells were cultured in vitro, and their DDP-resistant cells (8505C/DDP) were constructed. The proliferation ability of 8505C and 8505C/DDP cells that treated with 0, 25, 50, 75, and 100 nmol/L polydatin was detected by CCK-8 assay, in order to screen the optimal action concentration of polydatin. The 8505C cells were divided into control group, polydatin group, empty vector group, polydatin+YAP1 overexpression group; and the 8505C/DDP cells were divided into control group, DDP group, DDP+polydatin group, DDP+empty vector group, and DDP+polydatin+YAP1 overexpression group. WB assay was used to detect the expression of Hippo/YAP pathway related proteins [YAP1, transcriptional coactivator factor (TAZ)] and EMT-associated proteins (E-cadherin, N-cadherin) in the 8505C cells of each group; Besides, the expression levels of YAP1, TAZ, and drug resistance-associated proteins [P-glycoprotein (P-gp), multidrug resistance-associated protein 1 (MRP1)] as well as apoptosis-associated proteins (cleaved caspase-3, BAX, Bcl-2) in 8505C/DDP cells were also detected by WB. Transwell assay and cell scratching assay were used to detect the invasion and migration abilities of 8505C and 8505C/DDP cells in each group, respectively. Results: Polydatin significantly inhibited the proliferation of 8505C cells (P<0.05), but 8505C/DDP cells were resistant to low concentrations of polydatin (P<0.05). Moreover, polydatin significantly inhibited the protein expression of YAP1, TAZ and N-cadherin, elevated the protein expression of E-cadherin in 8505C cells (P<0.05), and significantly suppressed the migration and invasion of 8505C cells (all P<0.05); However, overexpression of YAP1 reversed the effects of polydatin on 8505C cells (all P<0.05). 50 nmo/L polydatin significantly inhibited the protein expression of YAP1, TAZ, P-gp, MRP1 and Bcl-2, elevated the protein expression of cleaved caspase-3 and BAX in 8505C/DDP cells which treated with DDP (all P<0.05), and induced cell apoptosis (all P<0.05); However, overexpression of YAP1 reversed the effect of polydatin on 8505C/DDP cells (all P<0.05). Conclusion: Polydatin inhibits the malignant biological behaviors and enhances the DDP-sensitivity of 8505C cells via inhibiting the Hippo/YAP signaling pathway.
Objective: To investigate the effect of polydatin on malignant biological behaviors and cisplatin(DDP) -sensitivity of human thyroid cancer 8505C cells by regulating the Hippo/Yes-associated protein (YAP) signaling pathway. Methods: 8505C cells were cultured in vitro, and their DDP-resistant cells (8505C/DDP) were constructed. The proliferation ability of 8505C and 8505C/DDP cells that treated with 0, 25, 50, 75, and 100 nmol/L polydatin was detected by CCK-8 assay, in order to screen the optimal action concentration of polydatin. The 8505C cells were divided into control group, polydatin group, empty vector group, polydatin+YAP1 overexpression group; and the 8505C/DDP cells were divided into control group, DDP group, DDP+polydatin group, DDP+empty vector group, and DDP+polydatin+YAP1 overexpression group. WB assay was used to detect the expression of Hippo/YAP pathway related proteins [YAP1, transcriptional coactivator factor (TAZ)] and EMT-associated proteins (E-cadherin, N-cadherin) in the 8505C cells of each group; Besides, the expression levels of YAP1, TAZ, and drug resistance-associated proteins [P-glycoprotein (P-gp), multidrug resistance-associated protein 1 (MRP1)] as well as apoptosis-associated proteins (cleaved caspase-3, BAX, Bcl-2) in 8505C/DDP cells were also detected by WB. Transwell assay and cell scratching assay were used to detect the invasion and migration abilities of 8505C and 8505C/DDP cells in each group, respectively. Results: Polydatin significantly inhibited the proliferation of 8505C cells (P<0.05), but 8505C/DDP cells were resistant to low concentrations of polydatin (P<0.05). Moreover, polydatin significantly inhibited the protein expression of YAP1, TAZ and N-cadherin, elevated the protein expression of E-cadherin in 8505C cells (P<0.05), and significantly suppressed the migration and invasion of 8505C cells (all P<0.05); However, overexpression of YAP1 reversed the effects of polydatin on 8505C cells (all P<0.05). 50 nmo/L polydatin significantly inhibited the protein expression of YAP1, TAZ, P-gp, MRP1 and Bcl-2, elevated the protein expression of cleaved caspase-3 and BAX in 8505C/DDP cells which treated with DDP (all P<0.05), and induced cell apoptosis (all P<0.05); However, overexpression of YAP1 reversed the effect of polydatin on 8505C/DDP cells (all P<0.05). Conclusion: Polydatin inhibits the malignant biological behaviors and enhances the DDP-sensitivity of 8505C cells via inhibiting the Hippo/YAP signaling pathway.
2024, 31(3):231-239.
DOI: 10.3872/j.issn.1007-385X.2024.03.004
Abstract:
Objective: To investigate the effect of miR-3612 targeting semaphorin (SEMA)4C on the proliferation and invasion ability of hepatocellular carcinoma cells. Methods: Forty pairs of cancerous tissues and corresponding paracancerous tissues of hepatocellular carcinoma that surgically resected at Yijishan Hospital, the First Affiliated Hospital of Wannan Medical College between May 2020 and September 2021 were collected for this study. Hepatocellular carcinoma Hep3B and Huh7 cells were routinely cultured and divided into control group, miR-3612 mimics-NC group, miR-3612 mimics group, miR-3612 inhibitor-NC group, miR-3612 inhibitor group, si-NC group, si-SEMA4C group, mimics-NC+pcDNA-NC group, miR-3612 mimics+pcDNA-NC group, and miR-3612 mimics+pcDNA- SEMA4C group. The corresponding nucleic acids and plasmids were transfected into each group of cells with transfection reagents.qPCR assay was used to detect the mRNA expression of miR-3612 and SEMA4C in hepatocellular carcinoma tissues and Hep3B and Huh7 cells. Dual-luciferase reporter gene assay and RNA immunoprecipitation assay (RIP) were used to validate the binding and regulatory relationship between miR-3612 and SEMA4C. qPCR and WB assays were used to detect the mRNA and protein expression of miR-3612 and SEMA4C in Hep3B and Huh7 cells after transfection in each group. The proliferation, migration and invasion abilities of Hep3B and Huh7 cells were detected by CCK-8 assay, cell scratch assay and Transwell assay, respectively. Results: miR-3612 was lowly expressed in hepatocellular carcinoma tissues and Hep3B and Huh7 cells (P<0.001), whereas SEMA4C was highly expressed (P<0.001). Overexpression of miR-3612 suppressed proliferation, migration, invasion, and expression of vimentin and SEMA4C proteins in Hep3B and Huh7 cells, promoted E-cadherin protein expression (P<0.05 or P<0.01 or P<0.001), and knockdown of miR-3612 promoted proliferation, migration, invasion and SEMA4C protein expression in Hep3B and Huh7 cells (P<0.05 or P<0.01 or P<0.001). Dual luciferase reporter gene assay and RIP assay confirmed that miR-3612 bound directly to SEMA4C (P<0.001), as indirectly evidenced by the negative correlation between miR-3612 and SEMA4C expression (P<0.001). Knockdown of SEMA4C significantly inhibited the proliferation, invasion and migration of Hep3B and Huh7 cells (P<0.05 or P<0.01 or P<0.001), and overexpression of SEMA4C reversed the inhibitory effect of miR-3612 overexpression on proliferation, migration, invasion and epithelial-mesenchymal transition (EMT) of Hep3B and Huh7 cells (P<0.05 or P<0.01 or P< 0.001). Conclusion: miR-3612 affects the malignant biological behaviors of Hep3B and Huh7 cells by regulating SEMA4C expression, and it is expected to be a potential target for clinical hepatocellular carcinoma therapy.
Objective: To investigate the effect of miR-3612 targeting semaphorin (SEMA)4C on the proliferation and invasion ability of hepatocellular carcinoma cells. Methods: Forty pairs of cancerous tissues and corresponding paracancerous tissues of hepatocellular carcinoma that surgically resected at Yijishan Hospital, the First Affiliated Hospital of Wannan Medical College between May 2020 and September 2021 were collected for this study. Hepatocellular carcinoma Hep3B and Huh7 cells were routinely cultured and divided into control group, miR-3612 mimics-NC group, miR-3612 mimics group, miR-3612 inhibitor-NC group, miR-3612 inhibitor group, si-NC group, si-SEMA4C group, mimics-NC+pcDNA-NC group, miR-3612 mimics+pcDNA-NC group, and miR-3612 mimics+pcDNA- SEMA4C group. The corresponding nucleic acids and plasmids were transfected into each group of cells with transfection reagents.qPCR assay was used to detect the mRNA expression of miR-3612 and SEMA4C in hepatocellular carcinoma tissues and Hep3B and Huh7 cells. Dual-luciferase reporter gene assay and RNA immunoprecipitation assay (RIP) were used to validate the binding and regulatory relationship between miR-3612 and SEMA4C. qPCR and WB assays were used to detect the mRNA and protein expression of miR-3612 and SEMA4C in Hep3B and Huh7 cells after transfection in each group. The proliferation, migration and invasion abilities of Hep3B and Huh7 cells were detected by CCK-8 assay, cell scratch assay and Transwell assay, respectively. Results: miR-3612 was lowly expressed in hepatocellular carcinoma tissues and Hep3B and Huh7 cells (P<0.001), whereas SEMA4C was highly expressed (P<0.001). Overexpression of miR-3612 suppressed proliferation, migration, invasion, and expression of vimentin and SEMA4C proteins in Hep3B and Huh7 cells, promoted E-cadherin protein expression (P<0.05 or P<0.01 or P<0.001), and knockdown of miR-3612 promoted proliferation, migration, invasion and SEMA4C protein expression in Hep3B and Huh7 cells (P<0.05 or P<0.01 or P<0.001). Dual luciferase reporter gene assay and RIP assay confirmed that miR-3612 bound directly to SEMA4C (P<0.001), as indirectly evidenced by the negative correlation between miR-3612 and SEMA4C expression (P<0.001). Knockdown of SEMA4C significantly inhibited the proliferation, invasion and migration of Hep3B and Huh7 cells (P<0.05 or P<0.01 or P<0.001), and overexpression of SEMA4C reversed the inhibitory effect of miR-3612 overexpression on proliferation, migration, invasion and epithelial-mesenchymal transition (EMT) of Hep3B and Huh7 cells (P<0.05 or P<0.01 or P< 0.001). Conclusion: miR-3612 affects the malignant biological behaviors of Hep3B and Huh7 cells by regulating SEMA4C expression, and it is expected to be a potential target for clinical hepatocellular carcinoma therapy.
2024, 31(3):240-246.
DOI: 10.3872/j.issn.1007-385X.2024.03.005
Abstract:
Objective: To investigate the effects of triptolide (TP) on the malignant biological behaviors of human breast cancer MCF-7 cells through the miR-142-3p/HSP70 signaling pathway. Methods: MCF-7 cells were routinely cultured and divided into 6 groups: control group, TP group, miR-142-3p inhibitor group, TP+inhibitor group, miR-142-3p mimics group and TP+mimics group. The corresponding nucleic acids or plasmids were transfected into MCF-7 cells with transfection reagents. The mRNA expression of miR-142-3p and HSP70 in MCF-7 cells was detected by qPCR method. The proliferation, invasion and migration abilities of MCF-7 cells were detected by EdU cell proliferation assay, Transwell chamber assay, and cell scratch assay, respectively. The protein expression of HSP70 in MCF-7 cells was determined by WB assay. Results: TP or miR-142-3p overexpression significantly promoted the expression of miR-142-3p and HSP70 in MCF-7 cells, while knockdown of miR-142-3p significantly inhibited the expression of miR-142-3p and HSP70 in MCF-7 cells. TP could reverse the effects of miR-142-3p knockdown on the expression of miR-142-3p and HSP70 in MCF-7 cells. TP and miR-142-3p overexpression could significantly inhibit the proliferation, migration and invasion of MCF-7 cells (all P<0.05), while knockdown of miR-142-3p could promote the proliferation, migration and invasion of MCF-7 cells (all P<0.05). TP could reverse the effect of miR-142-3p knockdown on the malignant biological behavior of MCF-7 cells (all P<0.05). Conclusions: TP can inhibit the proliferation, invasion, and migration of MCF-7 cells by regulating the miR-142-3p/HSP70 signaling pathway.
Objective: To investigate the effects of triptolide (TP) on the malignant biological behaviors of human breast cancer MCF-7 cells through the miR-142-3p/HSP70 signaling pathway. Methods: MCF-7 cells were routinely cultured and divided into 6 groups: control group, TP group, miR-142-3p inhibitor group, TP+inhibitor group, miR-142-3p mimics group and TP+mimics group. The corresponding nucleic acids or plasmids were transfected into MCF-7 cells with transfection reagents. The mRNA expression of miR-142-3p and HSP70 in MCF-7 cells was detected by qPCR method. The proliferation, invasion and migration abilities of MCF-7 cells were detected by EdU cell proliferation assay, Transwell chamber assay, and cell scratch assay, respectively. The protein expression of HSP70 in MCF-7 cells was determined by WB assay. Results: TP or miR-142-3p overexpression significantly promoted the expression of miR-142-3p and HSP70 in MCF-7 cells, while knockdown of miR-142-3p significantly inhibited the expression of miR-142-3p and HSP70 in MCF-7 cells. TP could reverse the effects of miR-142-3p knockdown on the expression of miR-142-3p and HSP70 in MCF-7 cells. TP and miR-142-3p overexpression could significantly inhibit the proliferation, migration and invasion of MCF-7 cells (all P<0.05), while knockdown of miR-142-3p could promote the proliferation, migration and invasion of MCF-7 cells (all P<0.05). TP could reverse the effect of miR-142-3p knockdown on the malignant biological behavior of MCF-7 cells (all P<0.05). Conclusions: TP can inhibit the proliferation, invasion, and migration of MCF-7 cells by regulating the miR-142-3p/HSP70 signaling pathway.
2024, 31(3):247-252.
DOI: 10.3872/j.issn.1007-385X.2024.03.006
Abstract:
Objective: To investigate whether pachymic acid (PA) affects the malignant biological behaviors of colorectal cancer (CRC) HCT116 cells through the AKT/MDM2/p53 pathway. Methods: HCT116 cells were routinely cultured and divided into control group, MK-2206 (AKT inhibitor) group, low PA concentration (PA-L) group, high PA concentration (PA-H) group, and PA-H+SC79 (AKT activator) group. CCK-8, Cell clone formation assay, flow cytometry and Transwell assay were used to detect the proliferation viability, clone formation ability, apoptosis, migration and invasion of HCT116 cells in each group. qPCR was used to determine the mRNA expression of E-cadherin, N-cadherin and vimentin, and WB assay was applied to detect the expression of AKT/MDM2/p53 pathway related proteins. Results: PA significantly suppressed the proliferation (P<0.05), clone formation ability, migration and invasion and induced apoptosis (all P<0.05) of HCT116 cells, inhibited the mRNA expression of N-cadherin and vimentin while promoted the mRNA expression of E-cadherin (all P<0.05), decreased the phosphorylation levels of AKT and MDM2 (both P<0.05),and elevated the protein expression of p53 (P<0.05) in HCT116 cells. The AKT inhibitor MK-2206 could mimic the effects of PA (all P<0.05), while its activator SC79 could reverse the effects of PA (all P<0.05). Conclusion: PA inhibits proliferation, migration and invasion and induces apoptosis of HCT116 cells by regulating the AKT/MDM2/p53 signaling pathway.
Objective: To investigate whether pachymic acid (PA) affects the malignant biological behaviors of colorectal cancer (CRC) HCT116 cells through the AKT/MDM2/p53 pathway. Methods: HCT116 cells were routinely cultured and divided into control group, MK-2206 (AKT inhibitor) group, low PA concentration (PA-L) group, high PA concentration (PA-H) group, and PA-H+SC79 (AKT activator) group. CCK-8, Cell clone formation assay, flow cytometry and Transwell assay were used to detect the proliferation viability, clone formation ability, apoptosis, migration and invasion of HCT116 cells in each group. qPCR was used to determine the mRNA expression of E-cadherin, N-cadherin and vimentin, and WB assay was applied to detect the expression of AKT/MDM2/p53 pathway related proteins. Results: PA significantly suppressed the proliferation (P<0.05), clone formation ability, migration and invasion and induced apoptosis (all P<0.05) of HCT116 cells, inhibited the mRNA expression of N-cadherin and vimentin while promoted the mRNA expression of E-cadherin (all P<0.05), decreased the phosphorylation levels of AKT and MDM2 (both P<0.05),and elevated the protein expression of p53 (P<0.05) in HCT116 cells. The AKT inhibitor MK-2206 could mimic the effects of PA (all P<0.05), while its activator SC79 could reverse the effects of PA (all P<0.05). Conclusion: PA inhibits proliferation, migration and invasion and induces apoptosis of HCT116 cells by regulating the AKT/MDM2/p53 signaling pathway.
CHEN Yan
,
ZHANG Yitian
,
XU Yan
,
LI Man
,
LI Jiawei
,
MENG Lingwen
,
XIANG Zheng
,
LIU Bing
,
YIN Zhinan
,
WU Bin
2024, 31(3):253-260.
DOI: 10.3872/j.issn.1007-385X.2024.03.007
Abstract:
Objective: To investigate the safety of allogeneic Vγ9Vδ2 T cell reinfusion therapy for advanced hepatocellular carcinoma (HCC) and the changes in the immune function of patients after treatment. Methods: Four advanced HCC patients admitted into Zhuhai People’ s Hospital between October, 2021 and October, 2022 were selected for the study. Peripheral blood mononuclear cells (PBMC) were obtained from healthy donors and Vγ9Vδ2 T cells were obtained after stimulation and amplification of PBMC. Vγ9Vδ2 T cells which passed quality control were reinfused. The dose of reinfused cells was 5×108 cells per time, once every two weeks, and reinfusions were carried out for more than 9 times. After treatments, the proportions of subgroup cells (αβT cells, B cells, NK cells and γδT cells) were detected. Biochemical markers of liver, kidney and heart function, such as transaminase, creatinine and creatine kinase were detected. Changes in the number of three types of cells in blood routine (the leukocyte system, the red blood cell system, and the platelet system) were detected. Results: After reinfusion treatment, all four patients showed good tolerance to allogeneic Vγ9Vδ2 T cells. Their biochemical markers of liver, kidney and heart functions, such as transaminase, creatinine and creatine kinase and the cell counts of three types of cells in blood routine showed no significant difference before and after reinfusion. Proportions of Tfh1, Tc1, CD127+ TEM, HLADR+CD8+ T cells, CD27-B cells increased, which indicated the enhancement of specific immunity. Conclusion: Allogeneic Vγ9Vδ2 T cell therapy for advanced HCC exhibits a good safety profile and can, to a certain extent, boost the patient's immune function.
Objective: To investigate the safety of allogeneic Vγ9Vδ2 T cell reinfusion therapy for advanced hepatocellular carcinoma (HCC) and the changes in the immune function of patients after treatment. Methods: Four advanced HCC patients admitted into Zhuhai People’ s Hospital between October, 2021 and October, 2022 were selected for the study. Peripheral blood mononuclear cells (PBMC) were obtained from healthy donors and Vγ9Vδ2 T cells were obtained after stimulation and amplification of PBMC. Vγ9Vδ2 T cells which passed quality control were reinfused. The dose of reinfused cells was 5×108 cells per time, once every two weeks, and reinfusions were carried out for more than 9 times. After treatments, the proportions of subgroup cells (αβT cells, B cells, NK cells and γδT cells) were detected. Biochemical markers of liver, kidney and heart function, such as transaminase, creatinine and creatine kinase were detected. Changes in the number of three types of cells in blood routine (the leukocyte system, the red blood cell system, and the platelet system) were detected. Results: After reinfusion treatment, all four patients showed good tolerance to allogeneic Vγ9Vδ2 T cells. Their biochemical markers of liver, kidney and heart functions, such as transaminase, creatinine and creatine kinase and the cell counts of three types of cells in blood routine showed no significant difference before and after reinfusion. Proportions of Tfh1, Tc1, CD127+ TEM, HLADR+CD8+ T cells, CD27-B cells increased, which indicated the enhancement of specific immunity. Conclusion: Allogeneic Vγ9Vδ2 T cell therapy for advanced HCC exhibits a good safety profile and can, to a certain extent, boost the patient's immune function.
2024, 31(3):261-270.
DOI: 10.3872/j.issn.1007-385X.2024.03.008
Abstract:
Objective: The classification of GINS family members based on their expression level in glioma tissue was explored to predict the prognosis of glioma patients, the efficacy of immunotherapy and the small molecules of traditional Chinese medicine. Methods: The database analyzed the relationship between GINS genomics, differentially expressed genes in glioma tissue and patient prognosis. Classification of gliomas based on gene expression of GINS family members and analysis of the prognosis of each subtype. Database data was analyzed for mutations, gene enrichment, tumor purity and immune cell infiltration scores for each subtype, as well as for Chinese traditional medicine small molecules that may interact with GINS2. Finally, the expression levels of GINS1~4 mRNA in Chinese human glioma tissues were detected by qPCR to verify their consistency with the database data. Results: GINS family members share similarities in gene, protein structure and function. Furthermore, they are highly expressed in glioma tissues and are strongly associated with poor patient prognosis (P<0.05). The classification of S1 and S2 subtypes based on the expression level of GINS family members in glioma tissue can better predict the prognosis of glioma patients. The main mutant genes of the S1 subtype are CDKN2A/B, EGFR and PTEN, while the mutant genes of the S2 subtype are IDH1, TP53 and ATRX. In addition, GINS family may affect the prognosis of glioma patients by regulating the immune microenvironment. CD276, and CX3CL1 may be potential targets for immunotherapy in patients with S1 subtype glioma. CHEMBL66033, 266935, 293914, 436859 and 1594881 May be the potential Chinese medicine small molecules targeting GINS2. Conclusion: The molecular typing of glioma constructed based on GINS family helps identify high-risk patients more suitable for immunotherapy, and the selected traditional Chinese medicine small molecules can provide a reference for molecular targeted therapy and immunotherapy for glioma patients.
Objective: The classification of GINS family members based on their expression level in glioma tissue was explored to predict the prognosis of glioma patients, the efficacy of immunotherapy and the small molecules of traditional Chinese medicine. Methods: The database analyzed the relationship between GINS genomics, differentially expressed genes in glioma tissue and patient prognosis. Classification of gliomas based on gene expression of GINS family members and analysis of the prognosis of each subtype. Database data was analyzed for mutations, gene enrichment, tumor purity and immune cell infiltration scores for each subtype, as well as for Chinese traditional medicine small molecules that may interact with GINS2. Finally, the expression levels of GINS1~4 mRNA in Chinese human glioma tissues were detected by qPCR to verify their consistency with the database data. Results: GINS family members share similarities in gene, protein structure and function. Furthermore, they are highly expressed in glioma tissues and are strongly associated with poor patient prognosis (P<0.05). The classification of S1 and S2 subtypes based on the expression level of GINS family members in glioma tissue can better predict the prognosis of glioma patients. The main mutant genes of the S1 subtype are CDKN2A/B, EGFR and PTEN, while the mutant genes of the S2 subtype are IDH1, TP53 and ATRX. In addition, GINS family may affect the prognosis of glioma patients by regulating the immune microenvironment. CD276, and CX3CL1 may be potential targets for immunotherapy in patients with S1 subtype glioma. CHEMBL66033, 266935, 293914, 436859 and 1594881 May be the potential Chinese medicine small molecules targeting GINS2. Conclusion: The molecular typing of glioma constructed based on GINS family helps identify high-risk patients more suitable for immunotherapy, and the selected traditional Chinese medicine small molecules can provide a reference for molecular targeted therapy and immunotherapy for glioma patients.
2024, 31(3):271-276.
DOI: 10.3872/j.issn.1007-385X.2024.03.009
Abstract:
Objective: To analyze the discriminative patterns of traditional Chinese medicine (TCM) in the non-interventional treatment of lung malignancies from a real-world perspective using data mining methods based on a clinical medical record information system. Methods: The medical history, symptoms at diagnosis, and medication information of patients with malignant lung cancer diagnosed in Dongzhimen Hospital of Beijing University of Chinese Medicine from January 1, 2015 to December 31, 2021 were collected from the medical record system, and a database was established after excluding the cases using interventional therapy. Microsoft Office Excel 2019 software was used to conduct descriptive statistics on the frequency, four basic properties and five tastes, meridian tropism, and efficacy of frequently used drugs. Microsoft Office Excel 2019 software was also used to data-mine the medical history and symptoms. Apriori algorithm in SPSS Modeler 18.0 software was applied to perform association rule analysis on the core data of high-frequency drugs and symptom information obtained from statistics, and an association network graph was constructed using web nodes. Cluster analysis was conducted using SPSS Statistics 23.0. Results: A total of 119 patients with malignant lung tumors who did not undergo interventional treatment were included. The common TCM symptoms included cough, white phlegm, wheezing, poor appetite, poor sleep, sticky phlegm, constipation, fatigue, chest tightness, and shortness of breath; Warm is the most common type among the four properties of the medicine; sweetness is the most common ype in the five flavors of the medicine; and the highest frequency of meridian tropism is lung meridian. The association rule results showed that the combinations with the highest support for binomial association were Pinellia ternata --??Chaihu, Pinellia ternata-Gualou, and Almond--Ephedra. The combinations with the highest support for trinomial association were Pinellia ternata--(Poria cocos, Bupleurum chinense), Almonds--(Ephedra, Pinellia ternate), Pinellia ternata- -(Almonds, Radix Bupleuri), and Pinellia ternata--(Gualou, Fritillaria).The clustering results revealed three clusters, namely phlegm heat obstructing lung syndrome, lung yin deficiency syndrome, and lung qi deficiency syndrome in succession. Conclusion: The discriminative patterns of TCM in the non-interventional treatment of malignant lung tumors were lung yin deficiency syndrome, phlegm heat obstructing lung syndrome and lung qi deficiency syndrome in the syndrome clusters. The treatment is mainly based on harmonizing Shaoyang, moving qi to relieve cough and asthma, and clearing deficiency heat and resolving phlegm-rheum. The commonly used drugs include Pinellia ternata, Glycyrrhiza, Scutellaria, Poria cocos, and Radix Bupleuri.
Objective: To analyze the discriminative patterns of traditional Chinese medicine (TCM) in the non-interventional treatment of lung malignancies from a real-world perspective using data mining methods based on a clinical medical record information system. Methods: The medical history, symptoms at diagnosis, and medication information of patients with malignant lung cancer diagnosed in Dongzhimen Hospital of Beijing University of Chinese Medicine from January 1, 2015 to December 31, 2021 were collected from the medical record system, and a database was established after excluding the cases using interventional therapy. Microsoft Office Excel 2019 software was used to conduct descriptive statistics on the frequency, four basic properties and five tastes, meridian tropism, and efficacy of frequently used drugs. Microsoft Office Excel 2019 software was also used to data-mine the medical history and symptoms. Apriori algorithm in SPSS Modeler 18.0 software was applied to perform association rule analysis on the core data of high-frequency drugs and symptom information obtained from statistics, and an association network graph was constructed using web nodes. Cluster analysis was conducted using SPSS Statistics 23.0. Results: A total of 119 patients with malignant lung tumors who did not undergo interventional treatment were included. The common TCM symptoms included cough, white phlegm, wheezing, poor appetite, poor sleep, sticky phlegm, constipation, fatigue, chest tightness, and shortness of breath; Warm is the most common type among the four properties of the medicine; sweetness is the most common ype in the five flavors of the medicine; and the highest frequency of meridian tropism is lung meridian. The association rule results showed that the combinations with the highest support for binomial association were Pinellia ternata --??Chaihu, Pinellia ternata-Gualou, and Almond--Ephedra. The combinations with the highest support for trinomial association were Pinellia ternata--(Poria cocos, Bupleurum chinense), Almonds--(Ephedra, Pinellia ternate), Pinellia ternata- -(Almonds, Radix Bupleuri), and Pinellia ternata--(Gualou, Fritillaria).The clustering results revealed three clusters, namely phlegm heat obstructing lung syndrome, lung yin deficiency syndrome, and lung qi deficiency syndrome in succession. Conclusion: The discriminative patterns of TCM in the non-interventional treatment of malignant lung tumors were lung yin deficiency syndrome, phlegm heat obstructing lung syndrome and lung qi deficiency syndrome in the syndrome clusters. The treatment is mainly based on harmonizing Shaoyang, moving qi to relieve cough and asthma, and clearing deficiency heat and resolving phlegm-rheum. The commonly used drugs include Pinellia ternata, Glycyrrhiza, Scutellaria, Poria cocos, and Radix Bupleuri.
2024, 31(3):277-282.
DOI: 10.3872/j.issn.1007-385X.2024.03.010
Abstract:
γδT细胞在肿瘤免疫治疗中具有重要潜力，其识别抗原的特异性和MHC非依赖性使其成为治疗的有力工具。然而， γδT细胞在肿瘤发生发展过程中发挥着复杂多样的双向作用，包括产生促进肿瘤生长的IL-17。近期的研究进一步揭示了γδT细胞的识别机制，包括Vγ9Vδ1 TCR 对EphA2的识别机制、Vγ9Vδ2 T细胞激活依赖于磷酸抗原（pAg）介导的BTN2A1-BTN3A1蛋白相互作用，以及TCR链介导的Vδ3亚群识别机制。这些发现为肿瘤免疫治疗提供了新思路，例如通过促进EphA2的表达来增强Vδ1T细胞的杀伤作用，通过干预BTN3A1-BTN2A1相互作用来控制Vγ9Vδ2 T细胞的异常活化等。随着对γδT细胞识别机制研究的不断深入，将为深入理解它们在免疫监视中的角色、优化肿瘤免疫治疗策略提供了新视角和有力支持。
γδT细胞在肿瘤免疫治疗中具有重要潜力，其识别抗原的特异性和MHC非依赖性使其成为治疗的有力工具。然而， γδT细胞在肿瘤发生发展过程中发挥着复杂多样的双向作用，包括产生促进肿瘤生长的IL-17。近期的研究进一步揭示了γδT细胞的识别机制，包括Vγ9Vδ1 TCR 对EphA2的识别机制、Vγ9Vδ2 T细胞激活依赖于磷酸抗原（pAg）介导的BTN2A1-BTN3A1蛋白相互作用，以及TCR链介导的Vδ3亚群识别机制。这些发现为肿瘤免疫治疗提供了新思路，例如通过促进EphA2的表达来增强Vδ1T细胞的杀伤作用，通过干预BTN3A1-BTN2A1相互作用来控制Vγ9Vδ2 T细胞的异常活化等。随着对γδT细胞识别机制研究的不断深入，将为深入理解它们在免疫监视中的角色、优化肿瘤免疫治疗策略提供了新视角和有力支持。
2024, 31(3):283-288.
DOI: 10.3872/j.issn.1007-385X.2024.03.011
Abstract:
T细胞活化V结构域免疫球蛋白抑制因子（VISTA）是一种新型免疫检查点蛋白，具有与B7家族相似但独特的结构。 VISTA在多种细胞中表达，包括髓系细胞和肿瘤细胞。在肿瘤中，VISTA可能通过调节髓系细胞和T细胞起到免疫抑制的作用。临床研究发现，VISTA在多种癌症中表达并与患者预后相关，可能是癌症治疗的潜在靶点，已有多种VISTA拮抗剂正在研发中。然而对VISTA分子机制和在免疫治疗中的确切作用仍需进一步研究。VISTA最新研究进展包括其与配体的相互作用以及其在肿瘤免疫治疗中的应用可能是免疫检查点抑制剂治疗实体肿瘤的新理论依据。
T细胞活化V结构域免疫球蛋白抑制因子（VISTA）是一种新型免疫检查点蛋白，具有与B7家族相似但独特的结构。 VISTA在多种细胞中表达，包括髓系细胞和肿瘤细胞。在肿瘤中，VISTA可能通过调节髓系细胞和T细胞起到免疫抑制的作用。临床研究发现，VISTA在多种癌症中表达并与患者预后相关，可能是癌症治疗的潜在靶点，已有多种VISTA拮抗剂正在研发中。然而对VISTA分子机制和在免疫治疗中的确切作用仍需进一步研究。VISTA最新研究进展包括其与配体的相互作用以及其在肿瘤免疫治疗中的应用可能是免疫检查点抑制剂治疗实体肿瘤的新理论依据。
2024, 31(3):289-295.
DOI: 10.3872/j.issn.1007-385X.2024.03.012
Abstract:
卵巢癌（OC）是最为致命的妇科恶性肿瘤，5年生存率仅为40%，而化疗耐药是影响OC患者预后的重要因素之一。研究发现糖代谢重编程参与肿瘤化疗耐药，其中涉及有氧糖酵解及磷酸戊糖途径代谢酶的过度表达而促进耐药，并且细胞氧化磷酸化状态也与化疗耐药密切相关，目前这些代谢途径中的关键分子已被用做新的药物靶点，并与传统抗肿瘤药物联合使用，在临床前研究中展现出良好的应用潜力。糖代谢重编程在OC化疗耐药中发挥重要作用，了解新型靶向代谢药物及其相关的治疗进展，对探索OC化疗耐药机制具有重要意义，可能为OC治疗提供新的治疗策略。
卵巢癌（OC）是最为致命的妇科恶性肿瘤，5年生存率仅为40%，而化疗耐药是影响OC患者预后的重要因素之一。研究发现糖代谢重编程参与肿瘤化疗耐药，其中涉及有氧糖酵解及磷酸戊糖途径代谢酶的过度表达而促进耐药，并且细胞氧化磷酸化状态也与化疗耐药密切相关，目前这些代谢途径中的关键分子已被用做新的药物靶点，并与传统抗肿瘤药物联合使用，在临床前研究中展现出良好的应用潜力。糖代谢重编程在OC化疗耐药中发挥重要作用，了解新型靶向代谢药物及其相关的治疗进展，对探索OC化疗耐药机制具有重要意义，可能为OC治疗提供新的治疗策略。
2024, 31(3):296-302.
DOI: 10.3872/j.issn.1007-385X.2024.03.013
Abstract:
随着基因工程和合成生物学的快速发展，以及对宿主病原体相互作用的认识更加深入，细菌在肿瘤治疗中的作用被广泛研究。细菌介导的肿瘤治疗机制主要包括肿瘤特异性靶向、诱发抗肿瘤免疫反应等，通过与化疗、放疗等传统疗法的结合，可以提高抗肿瘤疗效，同时降低对宿主的全身毒性。利用基因工程可获得对肿瘤组织更高靶向性的减毒菌株或细菌衍生物，从而提高肿瘤治疗的有效性和安全性。此外，细菌表面的可修饰性和表面化学偶联的多样性对实现理想载药及多模式抗肿瘤治疗成为可能，尤其是纳米载药体系与细菌结合组装的生物复合纳米递送系统，可克服传统纳米药物靶向性低、难以渗透到肿瘤深部组织的不足。尽管细菌用作抗肿瘤及释药体系的运输载体仍然有很多亟待解决的问题，但细菌在肿瘤区域特异性定植并诱导肿瘤免疫反应的特性以及作为理想药物载体的潜力，为肿瘤治疗提供了一个颇有前景的新范式。
随着基因工程和合成生物学的快速发展，以及对宿主病原体相互作用的认识更加深入，细菌在肿瘤治疗中的作用被广泛研究。细菌介导的肿瘤治疗机制主要包括肿瘤特异性靶向、诱发抗肿瘤免疫反应等，通过与化疗、放疗等传统疗法的结合，可以提高抗肿瘤疗效，同时降低对宿主的全身毒性。利用基因工程可获得对肿瘤组织更高靶向性的减毒菌株或细菌衍生物，从而提高肿瘤治疗的有效性和安全性。此外，细菌表面的可修饰性和表面化学偶联的多样性对实现理想载药及多模式抗肿瘤治疗成为可能，尤其是纳米载药体系与细菌结合组装的生物复合纳米递送系统，可克服传统纳米药物靶向性低、难以渗透到肿瘤深部组织的不足。尽管细菌用作抗肿瘤及释药体系的运输载体仍然有很多亟待解决的问题，但细菌在肿瘤区域特异性定植并诱导肿瘤免疫反应的特性以及作为理想药物载体的潜力，为肿瘤治疗提供了一个颇有前景的新范式。
2024, 31(3):303-309.
DOI: 10.3872/j.issn.1007-385X.2024.03.014
Abstract:
骨肉瘤是常见且高度恶性的原发性骨肿瘤，其治疗面临复发和转移的挑战，迫切需要探索新的骨肉瘤靶向治疗药物。该文聚焦于靶向新生血管形成的治疗策略，特别是针对血管内皮生长因子的抗血管生成治疗。综述了不同骨肉瘤抗血管生成药物在骨肉瘤治疗中的作用机制、临床效果及潜在的副作用。这些药物能有效抑制肿瘤增殖，但存在耐药性和不良反应的问题。通过对现有药物的分析和比较，为临床应用提供指导，并为骨肉瘤的治疗提供新思路。
骨肉瘤是常见且高度恶性的原发性骨肿瘤，其治疗面临复发和转移的挑战，迫切需要探索新的骨肉瘤靶向治疗药物。该文聚焦于靶向新生血管形成的治疗策略，特别是针对血管内皮生长因子的抗血管生成治疗。综述了不同骨肉瘤抗血管生成药物在骨肉瘤治疗中的作用机制、临床效果及潜在的副作用。这些药物能有效抑制肿瘤增殖，但存在耐药性和不良反应的问题。通过对现有药物的分析和比较，为临床应用提供指导，并为骨肉瘤的治疗提供新思路。
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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.