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Volume 30,Issue 9,2023 Table of Contents
2023, 30(9):745-753.
DOI: 10.3872/j.issn.1007-385X.2023.09.001
Abstract:
Tumor immunocytotherapy has shown promising clinical prospects. Recognition of tumor antigens by dendritic cells (DCs) is a critical initiating step in immune response. After capturing tumor antigens, DCs differentiate into mature cells and present the antigen signals to immune cells such as CD4+ T and CD8+ T cells in the lymph nodes, thereby stimulating an anti-tumor effect. This approach holds great potential for tumor treatment, especially for solid tumors. However, the complex structure of the solid tumor microenvironment and unclear mechanisms of DC and T/B cell immune response present significant challenges in front of us; therefore, the key theoretical and technological breakthroughs have not been achieved yet. Despite the advantages demonstrated by precise cellular immunotherapy such as CAR-T cells, antigen selection remains a bottleneck in treating solid tumors. DC-based therapeutic vaccines have shown promising efficacy and safety in clinical trials. With further elucidation of the important mechanisms of DCs in the TME, researchers have refocused on the anti-tumor effects of DCs. This has prompted the clinical transformation of DC combination therapies and synthetic biology vaccines for the treatment of solid tumors. Currently, DC-based clinical treatments for solid tumors are entering a new stage. This article provides a comprehensive review of the progress in clinical research on DC-based therapy for solid tumors, the types of DCs in TME and their anti-tumor mechanisms, engineered DC vaccines, as well as the existing challenges and coping strategies.
Tumor immunocytotherapy has shown promising clinical prospects. Recognition of tumor antigens by dendritic cells (DCs) is a critical initiating step in immune response. After capturing tumor antigens, DCs differentiate into mature cells and present the antigen signals to immune cells such as CD4+ T and CD8+ T cells in the lymph nodes, thereby stimulating an anti-tumor effect. This approach holds great potential for tumor treatment, especially for solid tumors. However, the complex structure of the solid tumor microenvironment and unclear mechanisms of DC and T/B cell immune response present significant challenges in front of us; therefore, the key theoretical and technological breakthroughs have not been achieved yet. Despite the advantages demonstrated by precise cellular immunotherapy such as CAR-T cells, antigen selection remains a bottleneck in treating solid tumors. DC-based therapeutic vaccines have shown promising efficacy and safety in clinical trials. With further elucidation of the important mechanisms of DCs in the TME, researchers have refocused on the anti-tumor effects of DCs. This has prompted the clinical transformation of DC combination therapies and synthetic biology vaccines for the treatment of solid tumors. Currently, DC-based clinical treatments for solid tumors are entering a new stage. This article provides a comprehensive review of the progress in clinical research on DC-based therapy for solid tumors, the types of DCs in TME and their anti-tumor mechanisms, engineered DC vaccines, as well as the existing challenges and coping strategies.
2023, 30(9):754-761.
DOI: 10.3872/j.issn.1007-385X.2023.09.002
Abstract:
To investigate the expression level, biological function and possible mechanism of LINC01503 in epithelial ovarian cancer (EOC). Methods: A total of 85 pairs of tumor tissues and fallopian tube tissues from EOC patients who underwent ovarian tumor reduction surgery in the Department of Gynecology, the Fourth Hospital of Hebei Medical University from May 2015 to May 2016 were collected. Human EOC cells A2780, SKOV3, OVCAR3 and OV90 and normal human ovarian epithelial cells IOSE80 were routinely cultured, and si-LINC01503, si-NC, and miR-342-3p mimic, miR mimic NC were transfected into SKOV3 and A2780 cells, respectively, and recorded as si-LINC01503 group, si-NC group, miR-342-3p mimic group and miR mimic NC group. qPCR was used to detect the expression level of LINC01503 in EOC tissues and cells, and Kaplan-Meier method was used to analyze the correlation between the expression of LINC01503 and the survival of EOC patients. Dual-luciferase reporter gene assay was used to verify the targeting relationship among melecules associated with LINC01503/miR-342-3p/IGF2R (insulin like growth factor 2 receptor) axis. The effects of LINC01503 knockdown and miR-342-3p over-expression on proliferation, migration and invasion of EOC A2780 and SKOV3 cells were detected by plate cloning assay, scratch wound healing assay and Transwell assay, respectively. The effect of LINC01503/miR-342-3p pathway on IGF2R protein expression was detected by WB method in SKOV3 and A2780 cells. A nude mouse model of A2780 cell transplanted tumor was established to observe the effect of LINC01503 on the growth of transplanted tumor. Results: The expression levels of LINC01503 in EOC tissues and cells were significantly higher than that in fallopian tube tissues and IOSE80 cells (all P<0.01). Kaplan-Meier survival analysis showed that compared with the low LINC01503 expression group, patients in the high LINC01503 expression group had significantly shorter PFS and OS after surgery (all P<0.01). Knockdown of LINC01503 and over-expression of miR-342-3p could inhibit proliferation, migration, and invasion of EOC cells (all P<0.01). WB results showed that knockdown of LINC01503 down-regulated the expression of IGF2R (P<0.01), which could be saved by transfection of miR-342-3p inhibitor (P<0.01). LINC01503 knockdown could inhibit the growth of A2780 cell transplanted tumors in vivo (P<0.01). Conclusion: LINC01503 is highly expressed in EOC tissues and cells, and it is significantly related to the poor prognosis of EOC patients. LINC01503 promotes the development of EOC possibly by upregulating IGF2R via sponging miR-342-3p.
To investigate the expression level, biological function and possible mechanism of LINC01503 in epithelial ovarian cancer (EOC). Methods: A total of 85 pairs of tumor tissues and fallopian tube tissues from EOC patients who underwent ovarian tumor reduction surgery in the Department of Gynecology, the Fourth Hospital of Hebei Medical University from May 2015 to May 2016 were collected. Human EOC cells A2780, SKOV3, OVCAR3 and OV90 and normal human ovarian epithelial cells IOSE80 were routinely cultured, and si-LINC01503, si-NC, and miR-342-3p mimic, miR mimic NC were transfected into SKOV3 and A2780 cells, respectively, and recorded as si-LINC01503 group, si-NC group, miR-342-3p mimic group and miR mimic NC group. qPCR was used to detect the expression level of LINC01503 in EOC tissues and cells, and Kaplan-Meier method was used to analyze the correlation between the expression of LINC01503 and the survival of EOC patients. Dual-luciferase reporter gene assay was used to verify the targeting relationship among melecules associated with LINC01503/miR-342-3p/IGF2R (insulin like growth factor 2 receptor) axis. The effects of LINC01503 knockdown and miR-342-3p over-expression on proliferation, migration and invasion of EOC A2780 and SKOV3 cells were detected by plate cloning assay, scratch wound healing assay and Transwell assay, respectively. The effect of LINC01503/miR-342-3p pathway on IGF2R protein expression was detected by WB method in SKOV3 and A2780 cells. A nude mouse model of A2780 cell transplanted tumor was established to observe the effect of LINC01503 on the growth of transplanted tumor. Results: The expression levels of LINC01503 in EOC tissues and cells were significantly higher than that in fallopian tube tissues and IOSE80 cells (all P<0.01). Kaplan-Meier survival analysis showed that compared with the low LINC01503 expression group, patients in the high LINC01503 expression group had significantly shorter PFS and OS after surgery (all P<0.01). Knockdown of LINC01503 and over-expression of miR-342-3p could inhibit proliferation, migration, and invasion of EOC cells (all P<0.01). WB results showed that knockdown of LINC01503 down-regulated the expression of IGF2R (P<0.01), which could be saved by transfection of miR-342-3p inhibitor (P<0.01). LINC01503 knockdown could inhibit the growth of A2780 cell transplanted tumors in vivo (P<0.01). Conclusion: LINC01503 is highly expressed in EOC tissues and cells, and it is significantly related to the poor prognosis of EOC patients. LINC01503 promotes the development of EOC possibly by upregulating IGF2R via sponging miR-342-3p.
2023, 30(9):762-770.
DOI: 10.3872/j.issn.1007-385X.2023.09.003
Abstract:
Objective：：To investigate the effect of LINC00462 binding to transcription factor MYC to activate ABCC3 on cisplatin sensitivity in clear cell renal cell carcinoma (ccRCC) and its potential mechanisms. Methods: The expression of ABCC3, MYC and LINC00462 and their correlation in ccRCC were analyzed, and the enrichment pathway of ABCC3 was also analyzed. Human renal tubular epithelial cells (HK-2) and ccRCC cells (A-498, 786-O and Caki-2) were conventionally cultured. Nucleic acid sequences of si-LINC00462,si-LINC00462-NC, oe-ABCC3, oe-ABCC3-NC, si-ABCC3, si-ABCC3-NC, si-MYC and si-MYC-NC were transfected into A-498 or 786-O cells respectively, namely si-LINC00462 group, si-LINC00462-NC group, oe-ABCC3 group, oe-ABCC3-NC group, si-ABCC3 group,si-ABCC3-NC group, si-MYC group and si-MYC-NC group. 2-deoxy-D-glucose (2-DG) was used in the rescue experiment, and oe-NC+PBS group, oe-ABCC3+PBS group and oe-ABCC3+2-DG group were established. To investigate the effects of LINC00462/MYC/ABCC3 axis on the cisplatin sensitivity of ccRCC cells, si-NC+oe-NC group, si-LINC00462+oe-NC gorup, and si-LINC00462+oe-ABCC3 group were constructed. The expression of ABCC3, MYC and LINC00462 in ccRCC cells was detected by qPCR. CCK-8 method was used to measure cell viability and the IC50 of cisplatin inhibiting the proliferation of ccRCC cells. WB was used to detect the expression of glycolytic metabolism-related proteins. Seahorse XP96 was used to analyze the extracellular acidification rate (ECAR) and oxygen consumption rate(OCR) in the cells of different treatment groups. The levels of pyruvate, lactic acid and ATP in the cells were detected by corresponding kits.The binding relationship between ABCC3 and MYC was verified by double luciferase reporter gene assay and chromatin immunoprecipitation (ChIP) assay, and the binding relationship between LINC00462 and MYC was verified using RNA-binding protein immunoprecipitation (RIP) experiment. Results: Database analysis and qPCR experiments showed that ABCC3 was highly expressed in ccRCC tissues and cells and was enriched in the glycolytic pathway. Knockdown of ABCC3 could promoted the sensitivity of A-498 cells to cisplatin, while overexpression of ABCC3 could reduce the sensitivity of 786-O cells to cisplatin. ABCC3 could inhibit the sensitivity of A-498 cells to cisplatin through promoting glycolysis. 2-DG treatment reversed the inhibitory effect of ABCC3 overexpression on cisplatin sensitivity of ccRCC cells. MYC could directly bind to ABCC3, and LINC00462 could recruit MYC. Knockdown of LINC00462 inhibited the expression of ABCC3, suppressed aerobic glycolysis of ccRCC cells and increased their sensitivity to cisplatin; however, further over-expression of ABCC3 reversed the effects of LINC00462 knockdown on inhibiting aerobic glycolysis and promoting cisplatin sensitivity in ccRCC cells. Conclusion：： LINC00462 promotes glycolysis of ccRCC cells and further inhibits their sensitivity to cisplatin by recruiting the transcription factor MYC to activate ABCC3 expression.
Objective：：To investigate the effect of LINC00462 binding to transcription factor MYC to activate ABCC3 on cisplatin sensitivity in clear cell renal cell carcinoma (ccRCC) and its potential mechanisms. Methods: The expression of ABCC3, MYC and LINC00462 and their correlation in ccRCC were analyzed, and the enrichment pathway of ABCC3 was also analyzed. Human renal tubular epithelial cells (HK-2) and ccRCC cells (A-498, 786-O and Caki-2) were conventionally cultured. Nucleic acid sequences of si-LINC00462,si-LINC00462-NC, oe-ABCC3, oe-ABCC3-NC, si-ABCC3, si-ABCC3-NC, si-MYC and si-MYC-NC were transfected into A-498 or 786-O cells respectively, namely si-LINC00462 group, si-LINC00462-NC group, oe-ABCC3 group, oe-ABCC3-NC group, si-ABCC3 group,si-ABCC3-NC group, si-MYC group and si-MYC-NC group. 2-deoxy-D-glucose (2-DG) was used in the rescue experiment, and oe-NC+PBS group, oe-ABCC3+PBS group and oe-ABCC3+2-DG group were established. To investigate the effects of LINC00462/MYC/ABCC3 axis on the cisplatin sensitivity of ccRCC cells, si-NC+oe-NC group, si-LINC00462+oe-NC gorup, and si-LINC00462+oe-ABCC3 group were constructed. The expression of ABCC3, MYC and LINC00462 in ccRCC cells was detected by qPCR. CCK-8 method was used to measure cell viability and the IC50 of cisplatin inhibiting the proliferation of ccRCC cells. WB was used to detect the expression of glycolytic metabolism-related proteins. Seahorse XP96 was used to analyze the extracellular acidification rate (ECAR) and oxygen consumption rate(OCR) in the cells of different treatment groups. The levels of pyruvate, lactic acid and ATP in the cells were detected by corresponding kits.The binding relationship between ABCC3 and MYC was verified by double luciferase reporter gene assay and chromatin immunoprecipitation (ChIP) assay, and the binding relationship between LINC00462 and MYC was verified using RNA-binding protein immunoprecipitation (RIP) experiment. Results: Database analysis and qPCR experiments showed that ABCC3 was highly expressed in ccRCC tissues and cells and was enriched in the glycolytic pathway. Knockdown of ABCC3 could promoted the sensitivity of A-498 cells to cisplatin, while overexpression of ABCC3 could reduce the sensitivity of 786-O cells to cisplatin. ABCC3 could inhibit the sensitivity of A-498 cells to cisplatin through promoting glycolysis. 2-DG treatment reversed the inhibitory effect of ABCC3 overexpression on cisplatin sensitivity of ccRCC cells. MYC could directly bind to ABCC3, and LINC00462 could recruit MYC. Knockdown of LINC00462 inhibited the expression of ABCC3, suppressed aerobic glycolysis of ccRCC cells and increased their sensitivity to cisplatin; however, further over-expression of ABCC3 reversed the effects of LINC00462 knockdown on inhibiting aerobic glycolysis and promoting cisplatin sensitivity in ccRCC cells. Conclusion：： LINC00462 promotes glycolysis of ccRCC cells and further inhibits their sensitivity to cisplatin by recruiting the transcription factor MYC to activate ABCC3 expression.
2023, 30(9):771-776.
DOI: 10.3872/j.issn.1007-385X.2023.09.004
Abstract:
Objective: To study the expression and biological function of low density lipoprotein receptor associated protein 11 (LRP11) in colorectal cancer (CRC) tissues and its effect on proliferation and apoptosis of CRC SW480 cells. Methods: The expression of LRP11 in CRC tissues in TCGA database was detected by bioinformatics tool. sh-LRP11 and sh-NC plasmids were transfected into SW480 cells by lentiviral infection technique, respectively. CCK-8 assay was used to detect cell viability, flow cytometry was used to detect cell apoptosis and cell cycle, and Western blot assay was used to detect the expression levels of cyclin D1, BAX, Bcl-2, β-catenin and active- β -catenin in the transfected cells. Results: As shown by TCGA database analysis, compared with normal tissues, the mRNA expression level of LRP11 in CRC tissues was significantly increased (P<0.05). Compared with sh-NC group, the proliferation activity of SW480 cells in sh-LRP11 group was obviously decreased (P<0.05), the apoptosis rate was significantly increased (P<0.01), and the mRNA expression of apoptosis-related protein BAX was increased (P<0.01), while the expression of Bcl-2 was decreased (P<0.01); moreover, the cells in G0/G1 phase was increased significantly and the cells in S-phase was decreased significantly (all P<0.01);meanwhile, the protein expression levels of cyclin D1 and β -catenin and active- β -catenin in wnt/β -catenin signaling pathway were significantly decreased (all P<0.01). Conclusion: The mRNA expression of LRP11 is highly expressed in CRC tissues, and interfering with LRP11 expression can inhibit the proliferation and promote the apoptosis of colon cancer SW480 cells, which provides a new therapeutic target for the treatment of CRC.
Objective: To study the expression and biological function of low density lipoprotein receptor associated protein 11 (LRP11) in colorectal cancer (CRC) tissues and its effect on proliferation and apoptosis of CRC SW480 cells. Methods: The expression of LRP11 in CRC tissues in TCGA database was detected by bioinformatics tool. sh-LRP11 and sh-NC plasmids were transfected into SW480 cells by lentiviral infection technique, respectively. CCK-8 assay was used to detect cell viability, flow cytometry was used to detect cell apoptosis and cell cycle, and Western blot assay was used to detect the expression levels of cyclin D1, BAX, Bcl-2, β-catenin and active- β -catenin in the transfected cells. Results: As shown by TCGA database analysis, compared with normal tissues, the mRNA expression level of LRP11 in CRC tissues was significantly increased (P<0.05). Compared with sh-NC group, the proliferation activity of SW480 cells in sh-LRP11 group was obviously decreased (P<0.05), the apoptosis rate was significantly increased (P<0.01), and the mRNA expression of apoptosis-related protein BAX was increased (P<0.01), while the expression of Bcl-2 was decreased (P<0.01); moreover, the cells in G0/G1 phase was increased significantly and the cells in S-phase was decreased significantly (all P<0.01);meanwhile, the protein expression levels of cyclin D1 and β -catenin and active- β -catenin in wnt/β -catenin signaling pathway were significantly decreased (all P<0.01). Conclusion: The mRNA expression of LRP11 is highly expressed in CRC tissues, and interfering with LRP11 expression can inhibit the proliferation and promote the apoptosis of colon cancer SW480 cells, which provides a new therapeutic target for the treatment of CRC.
2023, 30(9):777-783.
DOI: 10.3872/j.issn.1007-385X.2023.09.005
Abstract:
Objective: To evaluate the cell division cycle 20 gene (CDC20) expression in endometrial cancer (EC), and to explore the role and possible mechanism of CDC20 in regulating cell cycle and apoptosis of EC RL95-2 cells. Methods: The mRNA expression matrix of EC and matched patients' clinical information were acquired from The Cancer Genome Atlas (TCGA) database. The differential expression of CDC20 mRNA in EC and its correlation with tumor stage were analyzed with R package. Then, CDC20 expression in RL95-2 cells was detected with qPCR and WB assay. sh-CDC20 was transfected into RL95-2 cells to knockdown CDC20 expression. The effects of CDC20 knockdown on the cell proliferative viability, cell cycle distribution and cell apoptosis were measured with CCK-8 assay and flow cytometry, respectively, and its effect on the activity of Mcl-1/p-Chk1 axis was explored with WB assay. RL95-2 cell transplanted tumor model in nude mice was established to evaluate the anti-tumor effect of sh-CDC20 and its effect on apoptosis and Mcl-1/p-Chk1 axis in tumor tissues.Results: CDC20 was highly expressed in EC tissues and RL95-2 cells (P<0.01), and the high expression of CDC20 was strongly associated with EC tumor stage. Knockdown of CDC20 in RL95-2 cells could inhibit cell proliferative viability and cause cell cycle arrest at G1 phase (P<0.05 or P<0.01), promote cell apoptosis (P<0.01) and decrease the protein expressions of Mcl-1 and p-Chk1 in RL95-2 cells (P<0.05 or P<0.01). Knockdown of CDC20 remarkably inhibited the growth of xenografts in mice and reduced the expressions of Mcl-1 and p-Chk1 (all P<0.01), while promoted tumor cells apoptosis (P<0.01). Conclusion: CDC20 is highly expressed in EC tissues and is associated with tumor stage. Knockdown of CDC20 can inhibit the viability of RL95-2 cells and their transplanted tumors in nude mice and promote apoptosis, which may be related to the Mcl-1/p-Chk1 signaling axis.
Objective: To evaluate the cell division cycle 20 gene (CDC20) expression in endometrial cancer (EC), and to explore the role and possible mechanism of CDC20 in regulating cell cycle and apoptosis of EC RL95-2 cells. Methods: The mRNA expression matrix of EC and matched patients' clinical information were acquired from The Cancer Genome Atlas (TCGA) database. The differential expression of CDC20 mRNA in EC and its correlation with tumor stage were analyzed with R package. Then, CDC20 expression in RL95-2 cells was detected with qPCR and WB assay. sh-CDC20 was transfected into RL95-2 cells to knockdown CDC20 expression. The effects of CDC20 knockdown on the cell proliferative viability, cell cycle distribution and cell apoptosis were measured with CCK-8 assay and flow cytometry, respectively, and its effect on the activity of Mcl-1/p-Chk1 axis was explored with WB assay. RL95-2 cell transplanted tumor model in nude mice was established to evaluate the anti-tumor effect of sh-CDC20 and its effect on apoptosis and Mcl-1/p-Chk1 axis in tumor tissues.Results: CDC20 was highly expressed in EC tissues and RL95-2 cells (P<0.01), and the high expression of CDC20 was strongly associated with EC tumor stage. Knockdown of CDC20 in RL95-2 cells could inhibit cell proliferative viability and cause cell cycle arrest at G1 phase (P<0.05 or P<0.01), promote cell apoptosis (P<0.01) and decrease the protein expressions of Mcl-1 and p-Chk1 in RL95-2 cells (P<0.05 or P<0.01). Knockdown of CDC20 remarkably inhibited the growth of xenografts in mice and reduced the expressions of Mcl-1 and p-Chk1 (all P<0.01), while promoted tumor cells apoptosis (P<0.01). Conclusion: CDC20 is highly expressed in EC tissues and is associated with tumor stage. Knockdown of CDC20 can inhibit the viability of RL95-2 cells and their transplanted tumors in nude mice and promote apoptosis, which may be related to the Mcl-1/p-Chk1 signaling axis.
2023, 30(9):784-788.
DOI: 10.3872/j.issn.1007-385X.2023.09.006
Abstract:
Objective: To investigate the effect of 1, 25-dihydroxyvitamin D3 (VD3) on apoptosis of human breast cancer MCF-7 cells and its mechanism. Methods: Human breast cancer MCF-7 cells cultured in vitro were randomly divided into 6 groups: control group, 2-DG group, 1 μmol/L VD3 group, 10 μmol/L VD3 group, 2-DG+1 μmol/L VD3 group and 2-DG+10 μmol/L VD3 group. The cells in 6 groups were detected 48 h after they were treated with VD3 or 2-DG. The glucose uptake assay was used to measure the glucose uptake of cells, the ATP content in the cells was measured by the ATP kit, and the lactate level was measured by the lactate kit. The expression levels of cytochrome C (Cyt c) and apoptosis-associated proteins (Bcl-2, BAX, PARP1, caspase9 and caspase3) in MCF-7 cells were detected by WB method. Results: Compared with the control group, after the intervention of VD3, the apoptosis rate of MCF-7 cells increased significantly (P<0.05 or P<0.01), the glucose uptake, ATP content and lactate level were significantly decreased (P<0.05 or P<0.01), the expression of Cyt c, BAX, PARP1, caspase9 and caspase3 protein was significantly increased (all P<0.05), and the expression of Bcl-2 protein was decreased (P<0.05 or P<0.01); after the intervention of VD3 combined with 2-DG, the changes in the detection indexes of each group were more obvious (P<0.05 or P<0.01). Conclusion: VD3 can inhibit glycolysis of human breast cancer MCF-7 cells and induce apoptosis through the mitochondrial Cyt c pathway.
Objective: To investigate the effect of 1, 25-dihydroxyvitamin D3 (VD3) on apoptosis of human breast cancer MCF-7 cells and its mechanism. Methods: Human breast cancer MCF-7 cells cultured in vitro were randomly divided into 6 groups: control group, 2-DG group, 1 μmol/L VD3 group, 10 μmol/L VD3 group, 2-DG+1 μmol/L VD3 group and 2-DG+10 μmol/L VD3 group. The cells in 6 groups were detected 48 h after they were treated with VD3 or 2-DG. The glucose uptake assay was used to measure the glucose uptake of cells, the ATP content in the cells was measured by the ATP kit, and the lactate level was measured by the lactate kit. The expression levels of cytochrome C (Cyt c) and apoptosis-associated proteins (Bcl-2, BAX, PARP1, caspase9 and caspase3) in MCF-7 cells were detected by WB method. Results: Compared with the control group, after the intervention of VD3, the apoptosis rate of MCF-7 cells increased significantly (P<0.05 or P<0.01), the glucose uptake, ATP content and lactate level were significantly decreased (P<0.05 or P<0.01), the expression of Cyt c, BAX, PARP1, caspase9 and caspase3 protein was significantly increased (all P<0.05), and the expression of Bcl-2 protein was decreased (P<0.05 or P<0.01); after the intervention of VD3 combined with 2-DG, the changes in the detection indexes of each group were more obvious (P<0.05 or P<0.01). Conclusion: VD3 can inhibit glycolysis of human breast cancer MCF-7 cells and induce apoptosis through the mitochondrial Cyt c pathway.
2023, 30(9):789-796.
DOI: 10.3872/j.issn.1007-385X.2023.09.007
Abstract:
Objective: To investigate the effects of lycopene on the proliferation and apoptosis of renal carcinoma 786-O cells through silent information regulator 1 (SIRT1)/nuclear factor-kappa B (NF-κB) axis. Methods: Normal human kidney HK-2 cells and human renal cancer 786-O cells were conventionally cultured. The experiment included control group (0.1% DMSO), cisplatin group (40 μg/mL), lycopene low concentration (2.5 μ g/mL) group, lycopene high concentration (5 μ g/mL) group, and lycopene high concentration (5 μg/mL)+ EX527 (SIRT1 inhibitor) (3 μmol/L) group. The proliferation capacity of 786-O cells in each treatment group was detected by CCK-8 method and clonal formation assay. The apoptosis of HK-2 and 786-O cells in each treatment group was detected by flow cytometry. The changes of mitochondrial membrane potential and reactive oxygen species (ROS) in 786-O cells in each treatment group were detected by RH123 and DCFH-DA staining, respectively. The expression of apoptosis-related proteins, BAX, Bcl-2, C-casp3 and SIRT1/NF-κB axis-related proteins SIRT1 and p-NF-Κb, in 786-O cells were detected by WB method. The effects of low concentration lycopene (5 mg/kg), high concentration lycopene (20 mg/Kg), cisplatin (2 mg/kg), and lycopene (20 mg/kg) +EX527 (10 mg/kg) on the growth of 786-O cell transplanted tumor were observed. TUNEL method was used to detect the apoptosis in the tissues of transplanted tumors in each group. Results: Lycopene inhibited the proliferation activity of 786-O cells in a dose dependent manner. Lycopene and cisplatin significantly inhibited the clonogenesis ability of 786-O cells and promoted their apoptosis; moreover, after lycopene and cisplatin treatment, the MMP level was increased while ROS level was decreased, the expression of apoptosis-related proteins BAX and C-casp3 were significantly increased (all P<0.05), while the expression of Bcl-2 was down-regulated (P<0.05), the expression of SIRT1 was significantly increased (all P<0.05) and the expression of p-NF-κB was significantly decreased (all P<0.05). These effects could be reversed by EX527. Lycopene and cisplatin inhibited the growth of 786-O cell grafts in vivo and promoted the apoptosis of tumor cells,and their effects could also be reversed by EX527. Conclusion: Lycopene may inhibit the activation of NF-κB pathway through up-regulation of SIRT1, thus inhibiting proliferation of 786-O cells and inducing apoptosis.
Objective: To investigate the effects of lycopene on the proliferation and apoptosis of renal carcinoma 786-O cells through silent information regulator 1 (SIRT1)/nuclear factor-kappa B (NF-κB) axis. Methods: Normal human kidney HK-2 cells and human renal cancer 786-O cells were conventionally cultured. The experiment included control group (0.1% DMSO), cisplatin group (40 μg/mL), lycopene low concentration (2.5 μ g/mL) group, lycopene high concentration (5 μ g/mL) group, and lycopene high concentration (5 μg/mL)+ EX527 (SIRT1 inhibitor) (3 μmol/L) group. The proliferation capacity of 786-O cells in each treatment group was detected by CCK-8 method and clonal formation assay. The apoptosis of HK-2 and 786-O cells in each treatment group was detected by flow cytometry. The changes of mitochondrial membrane potential and reactive oxygen species (ROS) in 786-O cells in each treatment group were detected by RH123 and DCFH-DA staining, respectively. The expression of apoptosis-related proteins, BAX, Bcl-2, C-casp3 and SIRT1/NF-κB axis-related proteins SIRT1 and p-NF-Κb, in 786-O cells were detected by WB method. The effects of low concentration lycopene (5 mg/kg), high concentration lycopene (20 mg/Kg), cisplatin (2 mg/kg), and lycopene (20 mg/kg) +EX527 (10 mg/kg) on the growth of 786-O cell transplanted tumor were observed. TUNEL method was used to detect the apoptosis in the tissues of transplanted tumors in each group. Results: Lycopene inhibited the proliferation activity of 786-O cells in a dose dependent manner. Lycopene and cisplatin significantly inhibited the clonogenesis ability of 786-O cells and promoted their apoptosis; moreover, after lycopene and cisplatin treatment, the MMP level was increased while ROS level was decreased, the expression of apoptosis-related proteins BAX and C-casp3 were significantly increased (all P<0.05), while the expression of Bcl-2 was down-regulated (P<0.05), the expression of SIRT1 was significantly increased (all P<0.05) and the expression of p-NF-κB was significantly decreased (all P<0.05). These effects could be reversed by EX527. Lycopene and cisplatin inhibited the growth of 786-O cell grafts in vivo and promoted the apoptosis of tumor cells,and their effects could also be reversed by EX527. Conclusion: Lycopene may inhibit the activation of NF-κB pathway through up-regulation of SIRT1, thus inhibiting proliferation of 786-O cells and inducing apoptosis.
2023, 30(9):797-803.
DOI: 10.3872/j.issn.1007-385X.2023.09.008
Abstract:
Objective: To investigate the impacts of butorphanol (BPH) on the proliferation, migration and invasion of osteosarcoma (OS) cells and the relevant mechanism. Methods: MG-63 cells were grouped into a control group, a YAP inhibitor group (Verteporfin group), and low, medium and high concentration BPH groups. The cytotoxicity and proliferative activity of each group of cells were detected by MTT, the number of cell clones was detected by clonogenic assay, the apoptosis of cells was detected by flow cytometry, the migration ability of the cells was detected by wound-healing test, and the invasion ability of the cells was detected by Transwell assay. The mRNA expression of E-cadherin, N-cadherin and vimentin was detected by qPCR, and the protein expression of YAP and TAZ was detected by WB assay. Besides, the effects of BPH and verteporfin on growth of transplanted tumors were also observed. Results: Compared with the control group, the cell proliferation activity, the number of clones, the rate of wound healing, the number of invaded cells, the mRNA levels of N-cadherin and vimentin, the protein expression of YAP and TAZ, and the tumor volumes were obviously lower (all P<0.05), while the apoptosis rate, mRNA level of E-cadherin and the transplanted tumor inhibition rate were significantly higher (all P<0.05) in the Verteporfin group and the low, medium and high concentration BPH groups.There were no obvious differences in above observation indices between the high concentration BPH and the Verteporfin group (P>0.05). Conclusion: BPH may inhibit the proliferation, migration and invasion of OS cells by inhibiting Hippo/YAP signaling pathway.
Objective: To investigate the impacts of butorphanol (BPH) on the proliferation, migration and invasion of osteosarcoma (OS) cells and the relevant mechanism. Methods: MG-63 cells were grouped into a control group, a YAP inhibitor group (Verteporfin group), and low, medium and high concentration BPH groups. The cytotoxicity and proliferative activity of each group of cells were detected by MTT, the number of cell clones was detected by clonogenic assay, the apoptosis of cells was detected by flow cytometry, the migration ability of the cells was detected by wound-healing test, and the invasion ability of the cells was detected by Transwell assay. The mRNA expression of E-cadherin, N-cadherin and vimentin was detected by qPCR, and the protein expression of YAP and TAZ was detected by WB assay. Besides, the effects of BPH and verteporfin on growth of transplanted tumors were also observed. Results: Compared with the control group, the cell proliferation activity, the number of clones, the rate of wound healing, the number of invaded cells, the mRNA levels of N-cadherin and vimentin, the protein expression of YAP and TAZ, and the tumor volumes were obviously lower (all P<0.05), while the apoptosis rate, mRNA level of E-cadherin and the transplanted tumor inhibition rate were significantly higher (all P<0.05) in the Verteporfin group and the low, medium and high concentration BPH groups.There were no obvious differences in above observation indices between the high concentration BPH and the Verteporfin group (P>0.05). Conclusion: BPH may inhibit the proliferation, migration and invasion of OS cells by inhibiting Hippo/YAP signaling pathway.
9 Interaction between BCSG1 and Hsa-circ-0026352 in genetic susceptibility to invasive breast cancer
2023, 30(9):804-809.
DOI: 10.3872/j.issn.1007-385X.2023.09.009
Abstract:
Objective: To investigate the interaction between breast cancer specific gene 1 (BCSG1) and Hsa-circ-0026352 in genetic susceptibility of invasive breast cancer (IBC). Methods: 100 IBC patients admitted to Wuhan Hospital of Integrated Traditional Chinese and Western Medicine between June 2019 and May 2022 were selected as the study subjects, and the expression of BCSG1 in IBC tissues and their corresponding paracancerous tissues was detected by immunohistochemistry. The study subjects were classified into negative group, weakly positive group, and strongly positive group according to their protein expression level of BCSG1 in IBC tissues. The clinicopathological characteristics and expression of estrogen receptor (ER), progesterone receptor (PR), epidermal growth factor receptor-2 (HER-2) and Hsa-circ-0026352 of the patients in three groups were counted, and the trends and interactions of BCSG1 expression with the above parameters were analyzed using Logistic regression equations and maximum likelihood method. Results: The protein expression of BCSG1 was significantly higher in IBC tissues compared with the paracancerous tissues (P<0.05). Strong positive BCSG1 protein expression was associated with lymph node metastasis, differentiation degree, clinical stage, HER2 expression, and Hsa-circ-0026352 expression (all P<0.05). There was an interaction between strong positive BCSG1 expression and IBC (P<0.05). The interaction between BCSG1 expression and IBC was most significant in patients with positive Hsa-circ-0026352 expression (P<0.001). The interaction between BCSG1 expression and IBC was most significant in patients with clinical stage Ⅲ and low differentiation (all P<0.001). Conclusion: BCSG1 is closely related to IBC and interacts with Hsa-circ-0026352, clinical stage and degree of differentiation, which can collectively increase the risk of IBC.
Objective: To investigate the interaction between breast cancer specific gene 1 (BCSG1) and Hsa-circ-0026352 in genetic susceptibility of invasive breast cancer (IBC). Methods: 100 IBC patients admitted to Wuhan Hospital of Integrated Traditional Chinese and Western Medicine between June 2019 and May 2022 were selected as the study subjects, and the expression of BCSG1 in IBC tissues and their corresponding paracancerous tissues was detected by immunohistochemistry. The study subjects were classified into negative group, weakly positive group, and strongly positive group according to their protein expression level of BCSG1 in IBC tissues. The clinicopathological characteristics and expression of estrogen receptor (ER), progesterone receptor (PR), epidermal growth factor receptor-2 (HER-2) and Hsa-circ-0026352 of the patients in three groups were counted, and the trends and interactions of BCSG1 expression with the above parameters were analyzed using Logistic regression equations and maximum likelihood method. Results: The protein expression of BCSG1 was significantly higher in IBC tissues compared with the paracancerous tissues (P<0.05). Strong positive BCSG1 protein expression was associated with lymph node metastasis, differentiation degree, clinical stage, HER2 expression, and Hsa-circ-0026352 expression (all P<0.05). There was an interaction between strong positive BCSG1 expression and IBC (P<0.05). The interaction between BCSG1 expression and IBC was most significant in patients with positive Hsa-circ-0026352 expression (P<0.001). The interaction between BCSG1 expression and IBC was most significant in patients with clinical stage Ⅲ and low differentiation (all P<0.001). Conclusion: BCSG1 is closely related to IBC and interacts with Hsa-circ-0026352, clinical stage and degree of differentiation, which can collectively increase the risk of IBC.
2023, 30(9):810-816.
DOI: 10.3872/j.issn.1007-385X.2023.09.010
Abstract:
从20世纪90年代早期mRNA被首创性地应用于治疗性疫苗，到2020 年COVID-19大流行期间，mRNA疫苗的一鸣惊人，使得mRNA相关技术成为新一代疫苗候选者。mRNA疫苗正以前所未有的速度被应用到多个领域，让人们重燃对mRNA疫苗的热情和兴趣。由于其在灵活性、成本和开发速度方面的优势，该技术也为肿瘤治疗和个体化药物提供了巨大的利好。本文聚焦于mRNA肿瘤疫苗的DC、脂质载体等递送系统，总结了mRNA疫苗的优势及制备、应用等方面的研究进展，将有助于了解mRNA肿瘤疫苗的研发历程，为肿瘤疫苗提供新的思路和策略。
从20世纪90年代早期mRNA被首创性地应用于治疗性疫苗，到2020 年COVID-19大流行期间，mRNA疫苗的一鸣惊人，使得mRNA相关技术成为新一代疫苗候选者。mRNA疫苗正以前所未有的速度被应用到多个领域，让人们重燃对mRNA疫苗的热情和兴趣。由于其在灵活性、成本和开发速度方面的优势，该技术也为肿瘤治疗和个体化药物提供了巨大的利好。本文聚焦于mRNA肿瘤疫苗的DC、脂质载体等递送系统，总结了mRNA疫苗的优势及制备、应用等方面的研究进展，将有助于了解mRNA肿瘤疫苗的研发历程，为肿瘤疫苗提供新的思路和策略。
2023, 30(9):817-823.
DOI: 10.3872/j.issn.1007-385X.2023.09.011
Abstract:
自然杀伤（NK）细胞是固有免疫系统中发挥细胞毒性作用的淋巴细胞，而NKG2D是NK细胞最重要的活化性受体之一，它通过识别靶细胞表面的配体NKG2DL来传递活化信号并激活免疫细胞对靶细胞发挥杀伤作用，在肿瘤免疫治疗中发挥重要作用。肿瘤微环境（TME）内存在多种机制调节NKG2D和NKG2DL的表达，从而影响免疫系统对肿瘤细胞的清除并导致肿瘤逃逸。NKG2D的强激活作用及其配体NKG2DL在肿瘤细胞上的选择性表达，使NKG2D/NKG2DL轴成为肿瘤免疫治疗的潜在靶点。本文围绕NKG2D/NKG2DL 轴介导的免疫监视与逃逸的双重作用，揭示重塑TME 对肿瘤免疫的重要性；并就干预NKG2D/NKG2DL轴在肿瘤免疫治疗中的研究进展进行综述，为基于NKG2D/NKG2DL开发免疫治疗药物提供可靠依据和新思路。
自然杀伤（NK）细胞是固有免疫系统中发挥细胞毒性作用的淋巴细胞，而NKG2D是NK细胞最重要的活化性受体之一，它通过识别靶细胞表面的配体NKG2DL来传递活化信号并激活免疫细胞对靶细胞发挥杀伤作用，在肿瘤免疫治疗中发挥重要作用。肿瘤微环境（TME）内存在多种机制调节NKG2D和NKG2DL的表达，从而影响免疫系统对肿瘤细胞的清除并导致肿瘤逃逸。NKG2D的强激活作用及其配体NKG2DL在肿瘤细胞上的选择性表达，使NKG2D/NKG2DL轴成为肿瘤免疫治疗的潜在靶点。本文围绕NKG2D/NKG2DL 轴介导的免疫监视与逃逸的双重作用，揭示重塑TME 对肿瘤免疫的重要性；并就干预NKG2D/NKG2DL轴在肿瘤免疫治疗中的研究进展进行综述，为基于NKG2D/NKG2DL开发免疫治疗药物提供可靠依据和新思路。
2023, 30(9):824-829.
DOI: 10.3872/j.issn.1007-385X.2023.09.012
Abstract:
多药耐药现象是当前临床肿瘤治疗的主要障碍，且尚无有效的逆转方案。经过长期探索发现，细胞内药物外排增加、代谢增强、吸收下降、DNA突变及修复功能增强、肿瘤微环境影响等多种机制均参与了多药耐药现象的发生，且这些机制受转录因子、miRNA 及lncRNA 等因素的调控。当前研究者已开发出多种应对策略，包括小分子、中药逆转剂、纳米载体及生物疗法等进行耐药肿瘤治疗，但其疗效和生物安全性仍有待于进一步提升，深入的机制探索和多模态的治疗方案开发将是未来多药耐药肿瘤治疗的重要发展方向。
多药耐药现象是当前临床肿瘤治疗的主要障碍，且尚无有效的逆转方案。经过长期探索发现，细胞内药物外排增加、代谢增强、吸收下降、DNA突变及修复功能增强、肿瘤微环境影响等多种机制均参与了多药耐药现象的发生，且这些机制受转录因子、miRNA 及lncRNA 等因素的调控。当前研究者已开发出多种应对策略，包括小分子、中药逆转剂、纳米载体及生物疗法等进行耐药肿瘤治疗，但其疗效和生物安全性仍有待于进一步提升，深入的机制探索和多模态的治疗方案开发将是未来多药耐药肿瘤治疗的重要发展方向。
2023, 30(9):830-835.
DOI: 10.3872/j.issn.1007-385X.2023.09.013
Abstract:
上消化道恶性肿瘤（食管癌和胃癌）的发病率高，生存率低，严重威胁人类生命健康，具核梭杆菌（Fn）是一种常见的革兰氏阴性厌氧菌，被证明与多种疾病相关。近期的研究表明，Fn与上消化道恶性肿瘤具有潜在的相关性，Fn在癌组织中富集，可通过促进上皮间质转化（EMT）、抑制机体抗肿瘤免疫、干扰多胺代谢等多种作用机制增强肿瘤细胞的增殖、迁移能力及耐药性，从而调控肿瘤的发生发展，影响肿瘤的治疗效果及预后，靶向Fn 治疗可以提高治疗肿瘤的疗效和改善患者预后；而应用天青蛋白、噬菌体引导的生物治疗等方法可有效治疗Fn感染；目前，针对Fn的疫苗也正在开发中。阐明Fn在上消化道恶性肿瘤发生发展和治疗中的作用及其可能的机制，以及针对Fn 的治疗策略，将有助于上消化道恶性肿瘤的早期诊断，提供新的有效的预防和治疗策略。
上消化道恶性肿瘤（食管癌和胃癌）的发病率高，生存率低，严重威胁人类生命健康，具核梭杆菌（Fn）是一种常见的革兰氏阴性厌氧菌，被证明与多种疾病相关。近期的研究表明，Fn与上消化道恶性肿瘤具有潜在的相关性，Fn在癌组织中富集，可通过促进上皮间质转化（EMT）、抑制机体抗肿瘤免疫、干扰多胺代谢等多种作用机制增强肿瘤细胞的增殖、迁移能力及耐药性，从而调控肿瘤的发生发展，影响肿瘤的治疗效果及预后，靶向Fn 治疗可以提高治疗肿瘤的疗效和改善患者预后；而应用天青蛋白、噬菌体引导的生物治疗等方法可有效治疗Fn感染；目前，针对Fn的疫苗也正在开发中。阐明Fn在上消化道恶性肿瘤发生发展和治疗中的作用及其可能的机制，以及针对Fn 的治疗策略，将有助于上消化道恶性肿瘤的早期诊断，提供新的有效的预防和治疗策略。
2023, 30(9):836-841.
DOI: 10.3872/j.issn.1007-385X.2023.09.014
Abstract:
在乳腺癌的诊疗过程中，常规药物存在靶向性较差和严重的不良反应等缺陷。近年来，具有高选择性及优异成像性能的超顺磁性氧化铁纳米粒子（SPION）已成为影像学领域的研究热点。SPION 是一种具有磁性的纳米材料，其以氧化铁为核心，置于较弱的外磁场中就可产生较强的磁性。新型SPION 具有尺寸小、生物相容性好、制备流程简单和生产成本低等优点，且具有较好的磁响应能力，有望作为医学成像探针和药物靶向递送系统的载体，在提高肿瘤影像学特异性诊断和实现更精确给药等方面都具有良好的医学应用前景。在乳腺癌影像学诊断和治疗中，SPION 可作为分子靶向造影剂用于磁粒子成像观察，还可应用于化疗药物递送、基因传递、免疫治疗和光动力治疗等。随着以SPION为核心的临床试验进一步开展，SPION在乳腺癌诊疗中的应用将进一步拓展。
在乳腺癌的诊疗过程中，常规药物存在靶向性较差和严重的不良反应等缺陷。近年来，具有高选择性及优异成像性能的超顺磁性氧化铁纳米粒子（SPION）已成为影像学领域的研究热点。SPION 是一种具有磁性的纳米材料，其以氧化铁为核心，置于较弱的外磁场中就可产生较强的磁性。新型SPION 具有尺寸小、生物相容性好、制备流程简单和生产成本低等优点，且具有较好的磁响应能力，有望作为医学成像探针和药物靶向递送系统的载体，在提高肿瘤影像学特异性诊断和实现更精确给药等方面都具有良好的医学应用前景。在乳腺癌影像学诊断和治疗中，SPION 可作为分子靶向造影剂用于磁粒子成像观察，还可应用于化疗药物递送、基因传递、免疫治疗和光动力治疗等。随着以SPION为核心的临床试验进一步开展，SPION在乳腺癌诊疗中的应用将进一步拓展。
2023, 30(9):842-847.
DOI: 10.3872/j.issn.1007-385X.2023.09.015
Abstract:
靶向EGFR的抗体药物偶联物（EGFR-ADC）是由结合EGFR的单克隆抗体和细胞毒素偶联形成的兼具靶向性和高细胞毒性的新型肿瘤靶向药物。EGFR-ADC 能够靶向结合肿瘤细胞表面EGFR 受体，经细胞内化后依靠连接子裂解或抗体降解释放微管抑制剂、DNA 损伤剂等偶联的细胞毒素，从而发挥肿瘤杀伤作用，目前已有多个EGFR-ADC 已进入临床试验，部分在肿瘤的临床治疗中取得了显著疗效并批准上市。但是ADC 药物潜在的耐药性、不良反应以及复杂的内吞机制尚未完全阐明，总体上依然面临不良反应和疗效不足的问题，因此围绕ADC药物三大组分抗体（靶向、内化）、有效载荷（毒性效应）、连接子（载荷释放）的研发相继开展，而如何通过综合的优化设计以实现ADC药物的准确递送、高效内化、有效杀伤是当前的重要问题。因此，本文立足EGFR-ADC 药物的研发现状，针对其关键组分的结构设计、应用特点、作用机制进行综述分析，回顾总结代表性EGFR-ADC 的研究进展并对其耐药性和不良反应挑战以及相应对策进行了展望，以期为促进EGFR-ADC的开发和应用提供新思路。
靶向EGFR的抗体药物偶联物（EGFR-ADC）是由结合EGFR的单克隆抗体和细胞毒素偶联形成的兼具靶向性和高细胞毒性的新型肿瘤靶向药物。EGFR-ADC 能够靶向结合肿瘤细胞表面EGFR 受体，经细胞内化后依靠连接子裂解或抗体降解释放微管抑制剂、DNA 损伤剂等偶联的细胞毒素，从而发挥肿瘤杀伤作用，目前已有多个EGFR-ADC 已进入临床试验，部分在肿瘤的临床治疗中取得了显著疗效并批准上市。但是ADC 药物潜在的耐药性、不良反应以及复杂的内吞机制尚未完全阐明，总体上依然面临不良反应和疗效不足的问题，因此围绕ADC药物三大组分抗体（靶向、内化）、有效载荷（毒性效应）、连接子（载荷释放）的研发相继开展，而如何通过综合的优化设计以实现ADC药物的准确递送、高效内化、有效杀伤是当前的重要问题。因此，本文立足EGFR-ADC 药物的研发现状，针对其关键组分的结构设计、应用特点、作用机制进行综述分析，回顾总结代表性EGFR-ADC 的研究进展并对其耐药性和不良反应挑战以及相应对策进行了展望，以期为促进EGFR-ADC的开发和应用提供新思路。
2023, 30(9):848-850.
DOI: 10.3872/j.issn.1007-385X.2023.09.016
Abstract:
生物治疗学课程是随着生物医药行业发展而在很多医科院校开设的一门新课程，在培养行业人才中发挥着重要作用。新时代人才培养要求聚焦立德树人这一根本任务，用中国特色社会主义思想去“铸魂育人”，发挥思政教育对社会主义建设者和接班人培养的引领作用。本教学组在生物技术专业生物治疗学课程的教学实践中深入挖掘具有启迪性和教育性的思政元素，在理论知识与思政元素之间找到交叉点，并将其融入到课程的思政教育中，从多个角度探索实施生物治疗学课程思政教育的有效路径。本教学组将15个思政案例融入到生治疗学课程教学中。通过调查问卷的形式对课程思政实施的效果进行了评估，结果表明，此次课程思政教育的探索和改革取得了良好的教学效果。
生物治疗学课程是随着生物医药行业发展而在很多医科院校开设的一门新课程，在培养行业人才中发挥着重要作用。新时代人才培养要求聚焦立德树人这一根本任务，用中国特色社会主义思想去“铸魂育人”，发挥思政教育对社会主义建设者和接班人培养的引领作用。本教学组在生物技术专业生物治疗学课程的教学实践中深入挖掘具有启迪性和教育性的思政元素，在理论知识与思政元素之间找到交叉点，并将其融入到课程的思政教育中，从多个角度探索实施生物治疗学课程思政教育的有效路径。本教学组将15个思政案例融入到生治疗学课程教学中。通过调查问卷的形式对课程思政实施的效果进行了评估，结果表明，此次课程思政教育的探索和改革取得了良好的教学效果。
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- 《中国肿瘤生物治疗杂志》
- 1994年创刊
- 主办单位：Chinese Society of Immunology, Chinese Anti-cancer Association
- 邮编：200433
- 电话：021-81871002-22
- 电子邮箱：cjcb@biother.cn
- 网址:http://www.biother.cn
- 刊号：ISSN 1007-385X
- CN 31-1725/R
- 国内定价： ￥20元/册
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Chinese Journal Of Cancer Biotheray ® 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.