Mobile website
Volume 28,Issue 8,2021 Table of Contents
2021, 28(8):769-774.
DOI: 10.3872/j.issn.1007-385X.2021.08.001
Abstract:
In recent years, the development of tumor immunotherapy technology has made great contributions to broadening the field of precision tumor medicine. The immune microenvironment, which is an important factor that affects the treatment efficacy of immunotherapy, plays an indispensable role in tumor progression and mobilization of anti-tumor immunity. Immunity radiotherapy, immune checkpoint inhibitors, tumor vaccines, immune cell therapy, and other methods for the tumor immune microenvironment have achieved many results in clinical research, but their clinical efficacy still needs to be improved. This review introduces the composition and characteristics of the tumor immune microenvironment and expound the feasible optimization strategies for the current treatments targeting the immune microenvironment from the perspective of clinical application.
In recent years, the development of tumor immunotherapy technology has made great contributions to broadening the field of precision tumor medicine. The immune microenvironment, which is an important factor that affects the treatment efficacy of immunotherapy, plays an indispensable role in tumor progression and mobilization of anti-tumor immunity. Immunity radiotherapy, immune checkpoint inhibitors, tumor vaccines, immune cell therapy, and other methods for the tumor immune microenvironment have achieved many results in clinical research, but their clinical efficacy still needs to be improved. This review introduces the composition and characteristics of the tumor immune microenvironment and expound the feasible optimization strategies for the current treatments targeting the immune microenvironment from the perspective of clinical application.
2021, 28(8):775-782.
DOI: 10.3872/j.issn.1007-385X.2021.08.002
Abstract:
Objective: To detect the expression of lncRNA LOC440173 in NSCLC tissues and cells and to explore its influence on the maligant biological behavior of cancer cells. Methods: The cancer and para-cancerous tissues removed from 72 patients with NSCLC who were surgically during 2014 to 2017 in the biological specimen library of the Fourth Hospital of Hebei Medical University were selected. qPCR method was applied to detect the expression of LOC440173 in NSCLC tissues and the corresponding para-cancerous tissues as well as in six NSCLC cell lines (H520, H358, A549, HCC827, H1703 and H1299). The vectors used for LOC440173 knockdown or overexpression were constructed and transfected into H520 and H1703 cells, respectively. The effects of LOC440173 knockdown or overexpression on proliferation, migration, and invasion of lung cancer cells were examined by MTS, Clone formation, Transwell migration and invasion assays, respectively. qPCR method was used to detect the regulatory effect of LOC440173 on mRNA expression of EMT-related markers (E-cadherin, N-cadherin, and vimentin), WB method was employed to observe the protein expression of E-cadherin and N-cadherin. Results: The expression of LOC440173 in NSCLC tissues was significantly higher than that in corresponding para-cancerous tissues (P<0.01), and was correlated with lymph node metastasis, histological grade, TNM stage, and tumor size (P<0.05 or P<0.01). LOC440173 gene knockdown could inhibit the in vitro proliferation, invasion and migration of H520 cells (P<0.05 or P<0.01). Overexpression of LOC440173 gene significantly promoted the in vitro proliferation, migration, and invasion of H1703 cells (P<0.05 or P<0.01). At the transcriptional level, knockdown of LOC440173 was found to promote the expression level of E-cadherin and inhibit the expression level of N-cadherin and vimentin (P<0.05 or P<0.01), while overexpression of LOC440173 displayed the opposite results (P<0.05 or P<0.01). At the post-transcriptional level, LOC440173 negatively regulated protein expression of E-cadherin and positively modulated protein expression of N-cadherin (P<0.05). Conclusion: The abnormal high expression of LOC440173 may be related to the occurrence and development of NSCLC. LOC440173 can significantly improve the in vitro proliferation, migration and invasion of NSCLC cells, and the mechanism may be related to the regulation of EMT-related genes.
Objective: To detect the expression of lncRNA LOC440173 in NSCLC tissues and cells and to explore its influence on the maligant biological behavior of cancer cells. Methods: The cancer and para-cancerous tissues removed from 72 patients with NSCLC who were surgically during 2014 to 2017 in the biological specimen library of the Fourth Hospital of Hebei Medical University were selected. qPCR method was applied to detect the expression of LOC440173 in NSCLC tissues and the corresponding para-cancerous tissues as well as in six NSCLC cell lines (H520, H358, A549, HCC827, H1703 and H1299). The vectors used for LOC440173 knockdown or overexpression were constructed and transfected into H520 and H1703 cells, respectively. The effects of LOC440173 knockdown or overexpression on proliferation, migration, and invasion of lung cancer cells were examined by MTS, Clone formation, Transwell migration and invasion assays, respectively. qPCR method was used to detect the regulatory effect of LOC440173 on mRNA expression of EMT-related markers (E-cadherin, N-cadherin, and vimentin), WB method was employed to observe the protein expression of E-cadherin and N-cadherin. Results: The expression of LOC440173 in NSCLC tissues was significantly higher than that in corresponding para-cancerous tissues (P<0.01), and was correlated with lymph node metastasis, histological grade, TNM stage, and tumor size (P<0.05 or P<0.01). LOC440173 gene knockdown could inhibit the in vitro proliferation, invasion and migration of H520 cells (P<0.05 or P<0.01). Overexpression of LOC440173 gene significantly promoted the in vitro proliferation, migration, and invasion of H1703 cells (P<0.05 or P<0.01). At the transcriptional level, knockdown of LOC440173 was found to promote the expression level of E-cadherin and inhibit the expression level of N-cadherin and vimentin (P<0.05 or P<0.01), while overexpression of LOC440173 displayed the opposite results (P<0.05 or P<0.01). At the post-transcriptional level, LOC440173 negatively regulated protein expression of E-cadherin and positively modulated protein expression of N-cadherin (P<0.05). Conclusion: The abnormal high expression of LOC440173 may be related to the occurrence and development of NSCLC. LOC440173 can significantly improve the in vitro proliferation, migration and invasion of NSCLC cells, and the mechanism may be related to the regulation of EMT-related genes.
2021, 28(8):783-789.
DOI: 10.3872/j.issn.1007-385X.2021.08.003
Abstract:
Objective: To explore the effects of ultrasmall iron oxide nanoparticles (USIONPs) on the migration and invasion of human hepatocellular carcinoma HepG2 cells and its possible mechanism. Methods: The hydrate particle size and core particle size of USIONPs were analyzed by particle analysis device and transmission electron microscope, respectively. The dispersity and stability of USIONPs were characterized by Zeta potential and colloid stability analysis, respectively, to identify the successful prepaation of USIONPs. Different concentrations of USIONPs (0, 50, 100, 200 μg/ml) or 200 μg/ml USIONPs+5 mmol/L 3-MA (autophagy inhibitor) were used to treat human liver cancer HepG2 cells; then, CCK-8 assay was used to detect the proliferation viability of HepG2 cells; Transwell method was used to detect the migration and invasion ability of HepG2 cell; WB experiment was applied to detect the expression of autophagy markers Beclin1, LC3 and p62; 2',7'-dichlorodihydrofluorescein diacetic acid (DCFH-DA) method was used to determine the intracellular reactive oxygen species (ROS) level, and the iron ion colorimetric method was used to detect the iron ion level in the cells. Results: The average hydrate particle size of USIONPs was (37.86±12.90) nm, the core particle size was about 10 nm, and the Zeta potential was –23.8 mV, and confirmed the successful preparation of USIONP. The USIONPs had good water solubility and dispersibility. As the mass concentration of USIONPs increased and the incubation time prolonged, the proliferation viability of HepG2 cells showed a decreasing trend. Compared with the control group, after incubating HepG2 cells with 200 μg/ml USIONPs for 24 h, the numbers of migrated and invaded cells were significantly reduced (all P<0.05), and the addition of 3-MA could partially offset the above effects (P<0.05). Compared with the control group, the relative protein expression levels of beclin1 and LC3Ⅱin HepG2 cells in the 100 and 200 μg/ml USIONPs treatment groups increased significantly (all P<0.05), while the p62 protein expression decreased significantly (all P<0.05); 200 μg/ml USIONPs could significantly increase the level of intracellular ROS and iron ions, while the autophagy inhibitor 3-MA could block its effect (all P<0.05). Conclusion: USIONPs may promote autophagy of HepG2 cells, which consequently degrades USIONPs to release iron ions, leading to increased intracellular iron levels and ROS levels, thereby inhibiting the migration and invasion of HepG2 cells.
Objective: To explore the effects of ultrasmall iron oxide nanoparticles (USIONPs) on the migration and invasion of human hepatocellular carcinoma HepG2 cells and its possible mechanism. Methods: The hydrate particle size and core particle size of USIONPs were analyzed by particle analysis device and transmission electron microscope, respectively. The dispersity and stability of USIONPs were characterized by Zeta potential and colloid stability analysis, respectively, to identify the successful prepaation of USIONPs. Different concentrations of USIONPs (0, 50, 100, 200 μg/ml) or 200 μg/ml USIONPs+5 mmol/L 3-MA (autophagy inhibitor) were used to treat human liver cancer HepG2 cells; then, CCK-8 assay was used to detect the proliferation viability of HepG2 cells; Transwell method was used to detect the migration and invasion ability of HepG2 cell; WB experiment was applied to detect the expression of autophagy markers Beclin1, LC3 and p62; 2',7'-dichlorodihydrofluorescein diacetic acid (DCFH-DA) method was used to determine the intracellular reactive oxygen species (ROS) level, and the iron ion colorimetric method was used to detect the iron ion level in the cells. Results: The average hydrate particle size of USIONPs was (37.86±12.90) nm, the core particle size was about 10 nm, and the Zeta potential was –23.8 mV, and confirmed the successful preparation of USIONP. The USIONPs had good water solubility and dispersibility. As the mass concentration of USIONPs increased and the incubation time prolonged, the proliferation viability of HepG2 cells showed a decreasing trend. Compared with the control group, after incubating HepG2 cells with 200 μg/ml USIONPs for 24 h, the numbers of migrated and invaded cells were significantly reduced (all P<0.05), and the addition of 3-MA could partially offset the above effects (P<0.05). Compared with the control group, the relative protein expression levels of beclin1 and LC3Ⅱin HepG2 cells in the 100 and 200 μg/ml USIONPs treatment groups increased significantly (all P<0.05), while the p62 protein expression decreased significantly (all P<0.05); 200 μg/ml USIONPs could significantly increase the level of intracellular ROS and iron ions, while the autophagy inhibitor 3-MA could block its effect (all P<0.05). Conclusion: USIONPs may promote autophagy of HepG2 cells, which consequently degrades USIONPs to release iron ions, leading to increased intracellular iron levels and ROS levels, thereby inhibiting the migration and invasion of HepG2 cells.
2021, 28(8):790-795.
DOI: 10.3872/j.issn.1007-385X.2021.08.004
Abstract:
Objective: To explore the effects of long-chain non-coding RNA (lncRNA) FAM95B1 on the proliferation and migration of glioma cells and explore its related mechanisms. Methods: The glioma tissues and corresponding para-cancerous tissues of 38 glioma patients who underwent surgical treatment in The Third People's Hospital of Hefei from January 2018 to August 2020 were selected for this study. qPCR was used to detect the expression level of FAM95B1 in glioma tissues and cell lines. LN382 cells with the lowest FAM95B1 expression were used as the research object and transfected with empty plasmid (control group) or pcDNA3.1-FAM95B1 plasmid (experimental group). MTT assay and Scratch test were used to detect the effect of FAM95B1 on the proliferation and migration of LN382 cells. Bioinformatics tools were used to predict the relationship among FAM95B1, miR-26a-5p, and the phosphatase and tensin homology deleted on chromosome ten (PTEN), which was further verified by Dual-luciferase reporter gene assay. qPCR and Western blotting were used to detect the effect of FAM95B1 on the expression of miR-26a-5p and PTEN. Results:The expression of FAM95B1 in glioma tissues was significantly lower than that in para-cancerous tissues (P<0.01). The expression of FAM95B1 in various glioma cell lines was significantly lower than that in normal brain glial cells (all P<0.01). Overexpression of FAM95B1 could inhibit the proliferation (P<0.05) and migration ability (P<0.01) of LN382 cells. FAM95B1 could complementarily bind with miR-26a-5p (P<0.01), and miR-26a-5p could complementarily bind with PTEN mRNA (P<0.01). Overexpression of FAM95B1 could down-regulate the expression of miR-26a-5p (P<0.01)，and promote the mRNA and protein expression of PTEN (P<0.01) in LN382 cells. Conclusion: The abnormally low expression of FAM95B1 in glioma tissues and cell lines inhibits the expression of miR-26a-5p by exerting the function of competitive endogenous RNA to enhance PTEN gene expression, and inhibits the proliferation and migration of glioma cell line LN382.
Objective: To explore the effects of long-chain non-coding RNA (lncRNA) FAM95B1 on the proliferation and migration of glioma cells and explore its related mechanisms. Methods: The glioma tissues and corresponding para-cancerous tissues of 38 glioma patients who underwent surgical treatment in The Third People's Hospital of Hefei from January 2018 to August 2020 were selected for this study. qPCR was used to detect the expression level of FAM95B1 in glioma tissues and cell lines. LN382 cells with the lowest FAM95B1 expression were used as the research object and transfected with empty plasmid (control group) or pcDNA3.1-FAM95B1 plasmid (experimental group). MTT assay and Scratch test were used to detect the effect of FAM95B1 on the proliferation and migration of LN382 cells. Bioinformatics tools were used to predict the relationship among FAM95B1, miR-26a-5p, and the phosphatase and tensin homology deleted on chromosome ten (PTEN), which was further verified by Dual-luciferase reporter gene assay. qPCR and Western blotting were used to detect the effect of FAM95B1 on the expression of miR-26a-5p and PTEN. Results:The expression of FAM95B1 in glioma tissues was significantly lower than that in para-cancerous tissues (P<0.01). The expression of FAM95B1 in various glioma cell lines was significantly lower than that in normal brain glial cells (all P<0.01). Overexpression of FAM95B1 could inhibit the proliferation (P<0.05) and migration ability (P<0.01) of LN382 cells. FAM95B1 could complementarily bind with miR-26a-5p (P<0.01), and miR-26a-5p could complementarily bind with PTEN mRNA (P<0.01). Overexpression of FAM95B1 could down-regulate the expression of miR-26a-5p (P<0.01)，and promote the mRNA and protein expression of PTEN (P<0.01) in LN382 cells. Conclusion: The abnormally low expression of FAM95B1 in glioma tissues and cell lines inhibits the expression of miR-26a-5p by exerting the function of competitive endogenous RNA to enhance PTEN gene expression, and inhibits the proliferation and migration of glioma cell line LN382.
2021, 28(8):796-802.
DOI: 10.3872/j.issn.1007-385X.2021.08.005
Abstract:
Objective: To explore the effects of regorafenib (Rego) on proliferation and apoptosis of human liver cancer SMMC-7721 cells and the possible mechanism. Methods: SMMC-7721 cells were divided into control group and Rego group (10 μmol/L Rego).After the treatment for 48 h, Flow cytometry was used to detect cell apoptosis rate, and qPCR was used to determine the level of miR-122 in two groups of cells. hsa-miR-122-5p mimics were transfected into SMMC-7721 cells by lipofection to construct the miR-122 overexpressing cell line (overExp-miR-122). Then, the cells were divided into control group, Rego group, overExp-NC group,overExp-NC+Rego group, overExp-miR-122 group and overExp-miR-122+Rego group. MTT and Flow cytometry were used to detect cell viability and apoptosis rate, respectively. The protein expression levels of Bcl2, cleaved caspase-3, RAS, RAF1 and p-ERK1 in cells were detected by WB assay. Results: Compared with control group, the cell apoptosis rate was significantly increased after Rego treatment (P<0.05), and miR-122 expression level was significantly increased in Rego group (P<0.01). Compared with overExp-NC group, the proliferation inhibition rate and apoptosis rate in the cells of overExp-miR-122 group were significantly increased (P<0.01),the expression level of cleaved caspase-3 was significantly upregulated, while the protein expressions of Bcl2, RAS, RAF and p-ERK were significantly decreased (P<0.05 or P<0.01). Compared with overExp-miR-122 group, the changes in above detected indicators of overExp-miR-122+Rego group were more obvious (P<0.01). Conclusion: Regorafenib can inhibit the proliferation and promote apoptosis of SMMC-7721 cells, which may be achieved by regulating the expression of miR-122, thereby regulating the expression of apoptosis related factors and inhibiting RAS/RAF/ERK signaling pathway.
Objective: To explore the effects of regorafenib (Rego) on proliferation and apoptosis of human liver cancer SMMC-7721 cells and the possible mechanism. Methods: SMMC-7721 cells were divided into control group and Rego group (10 μmol/L Rego).After the treatment for 48 h, Flow cytometry was used to detect cell apoptosis rate, and qPCR was used to determine the level of miR-122 in two groups of cells. hsa-miR-122-5p mimics were transfected into SMMC-7721 cells by lipofection to construct the miR-122 overexpressing cell line (overExp-miR-122). Then, the cells were divided into control group, Rego group, overExp-NC group,overExp-NC+Rego group, overExp-miR-122 group and overExp-miR-122+Rego group. MTT and Flow cytometry were used to detect cell viability and apoptosis rate, respectively. The protein expression levels of Bcl2, cleaved caspase-3, RAS, RAF1 and p-ERK1 in cells were detected by WB assay. Results: Compared with control group, the cell apoptosis rate was significantly increased after Rego treatment (P<0.05), and miR-122 expression level was significantly increased in Rego group (P<0.01). Compared with overExp-NC group, the proliferation inhibition rate and apoptosis rate in the cells of overExp-miR-122 group were significantly increased (P<0.01),the expression level of cleaved caspase-3 was significantly upregulated, while the protein expressions of Bcl2, RAS, RAF and p-ERK were significantly decreased (P<0.05 or P<0.01). Compared with overExp-miR-122 group, the changes in above detected indicators of overExp-miR-122+Rego group were more obvious (P<0.01). Conclusion: Regorafenib can inhibit the proliferation and promote apoptosis of SMMC-7721 cells, which may be achieved by regulating the expression of miR-122, thereby regulating the expression of apoptosis related factors and inhibiting RAS/RAF/ERK signaling pathway.
2021, 28(8):803-809.
DOI: 10.3872/j.issn.1007-385X.2021.08.006
Abstract:
Objective: To investigate the effect of Urtica dioica extract on the proliferation, apoptosis, and cell cycle of breast cancer cells, and to primarily explore the possible mechanism. Methods: Breast cancer MCF-7 and MDA-MB-231 cells were treated with different concentrations of Urtica dioica extract (0,1,2,4,8,16,32,64 mg/ml) for 24 h, and the cell viability was detected by MTT. The concentrations around the median inhibitory concentration, which were 5 and 10 mg/ml, were selected to treat MCF-7 and MDA-MB-231 cells for 24 h, respectively. Plate clone formation assay was applied to detect cell proliferation, Flow cytometry was used to detect cell cycle and apoptosis, and WB was used to determine the expression of cell cycle and apoptosis-related proteins as well as PI3K/AKT signaling pathway-related proteins. AKT was simultaneously overexpressed in MCF-7 cells that were treated with 5 mg/ml Urtica dioica extract (Urtica+AKT group), and the cells transfected with empty vectors was used as control group (Urtica+vec group). The overexpression efficiency was detected by WB, and the effects of AKT overexpression on cell proliferation, cell cycle, and apoptosis were explored. Results: The viability of MCF-7 and MDA-MB-231 cells in each Urtica treated group was significantly lower than that in the control group (P<0.05, P<0.01). Compared with the control group, the number of clone formation of breast cancer cells was significantly reduced, while the proportion of cells in the G0/G1 phase and the apoptosis rate were significantly increased in the 5 or 10 mg/ml Urtica treatment groups (P<0.05, P<0.01); in addition, the protein expression of P21 and Bax was significantly increased,while the protein expression of Cyclin D1, CDK4, Bcl2, p-PI3K and p-AKT was significantly decreased (P<0.05, P<0.01) in Urtica treatment groups. The protein expression of p-AKT and AKT in the Urtica+AKT group was significantly higher than that in the Urtica+vec group, and the number of clone formation and proportion of cells in the S phase and G2/M phase were higher than that in the Urtica+vec group, and the proportion of cells in the G0/G1 phase and the apoptosis rate were lower than that in the Urtica+vec group (P<0.05, P<0.01). Conclusion: The Urtica dioica extract can inhibit the proliferation and promote the apoptosis of breast cancer cells,and block the cells at G0/G1 phase, the mechanism of which may be related to the inhibition of PI3K/AKT signaling pathway.
Objective: To investigate the effect of Urtica dioica extract on the proliferation, apoptosis, and cell cycle of breast cancer cells, and to primarily explore the possible mechanism. Methods: Breast cancer MCF-7 and MDA-MB-231 cells were treated with different concentrations of Urtica dioica extract (0,1,2,4,8,16,32,64 mg/ml) for 24 h, and the cell viability was detected by MTT. The concentrations around the median inhibitory concentration, which were 5 and 10 mg/ml, were selected to treat MCF-7 and MDA-MB-231 cells for 24 h, respectively. Plate clone formation assay was applied to detect cell proliferation, Flow cytometry was used to detect cell cycle and apoptosis, and WB was used to determine the expression of cell cycle and apoptosis-related proteins as well as PI3K/AKT signaling pathway-related proteins. AKT was simultaneously overexpressed in MCF-7 cells that were treated with 5 mg/ml Urtica dioica extract (Urtica+AKT group), and the cells transfected with empty vectors was used as control group (Urtica+vec group). The overexpression efficiency was detected by WB, and the effects of AKT overexpression on cell proliferation, cell cycle, and apoptosis were explored. Results: The viability of MCF-7 and MDA-MB-231 cells in each Urtica treated group was significantly lower than that in the control group (P<0.05, P<0.01). Compared with the control group, the number of clone formation of breast cancer cells was significantly reduced, while the proportion of cells in the G0/G1 phase and the apoptosis rate were significantly increased in the 5 or 10 mg/ml Urtica treatment groups (P<0.05, P<0.01); in addition, the protein expression of P21 and Bax was significantly increased,while the protein expression of Cyclin D1, CDK4, Bcl2, p-PI3K and p-AKT was significantly decreased (P<0.05, P<0.01) in Urtica treatment groups. The protein expression of p-AKT and AKT in the Urtica+AKT group was significantly higher than that in the Urtica+vec group, and the number of clone formation and proportion of cells in the S phase and G2/M phase were higher than that in the Urtica+vec group, and the proportion of cells in the G0/G1 phase and the apoptosis rate were lower than that in the Urtica+vec group (P<0.05, P<0.01). Conclusion: The Urtica dioica extract can inhibit the proliferation and promote the apoptosis of breast cancer cells,and block the cells at G0/G1 phase, the mechanism of which may be related to the inhibition of PI3K/AKT signaling pathway.
2021, 28(8):810-817.
DOI: 10.3872/j.issn.1007-385X.2021.08.007
Abstract:
Objective: To investigate the expression of forkhead box protein D3 (FOXD3) in gastric cardia adenocarcinoma (GCA) and its effect on the biological behaviors of SGC-7901 cells. Methods: A total of 49 pairs of GCA tissues and corresponding para[1]cancerous tissues that surgically resected from June 2014 to December 2016 were selected from the Biological Specimen Library of the Fourth Hospital of Hebei Medical University. qRT-PCR was used to detect the expression of FOXD3 in GCA tissues and corresponding para-cancerous tissues, as well as in gastric cancer cell lines（BGC-823, SGC-7901, HGC-27, MGC-803, and NCI-N87）. pc-DNA3.1-FOXD3 or pc-DNA3.1 was transfected into SGC-7901 cells. Cell proliferation assay, clone formation assay, scratch healing assay, and Transwell chamber invasion assay were used to detected the effect of FOXD3 overexpression on the the proliferation, clone formation,migration, and invasion of SGC-7901 cells. The mRNA and protein expressions of epithelial-mesenchymal transition (EMT) related molecules before and after the transfection were detected by qRT-PCR and WB. Cell cycle changes before and after transfection were detected by Flow cytometry. Results: The expression of FOXD3 mRNA in GCA tissues was significantly downregulated, and it's expression was closely correlated with clinical stage and lymph node metastasis of GCA patients. The expression of FOXD3 in gastric cancer cell lines was lower than that in normal cell lines (all P<0.01). FOXD3 overexpression significantly inhibited the proliferation,clone formation, migration and invasion of SGC-7901 cells in vitro (all P<0.01). FOXD3 overexpression could up-regulate the expression of E-cadherin and down-regulate the expressions of N-cadherin, β -catenin and vimentin in SGC-7901 cells (all P<0.01). Overexpression of FOXD3 could arrest the cell cycle in the G0/G1 phase (P<0.01). Conclusion: The expression of FOXD3 in GCA tissues is significantly downregulated, and its overexpression can inhibit the biological behaviors of gastric cancer cells. FOXD3 can be used as a tumor suppressor gene to provide new ideas for tumor therapy.
Objective: To investigate the expression of forkhead box protein D3 (FOXD3) in gastric cardia adenocarcinoma (GCA) and its effect on the biological behaviors of SGC-7901 cells. Methods: A total of 49 pairs of GCA tissues and corresponding para[1]cancerous tissues that surgically resected from June 2014 to December 2016 were selected from the Biological Specimen Library of the Fourth Hospital of Hebei Medical University. qRT-PCR was used to detect the expression of FOXD3 in GCA tissues and corresponding para-cancerous tissues, as well as in gastric cancer cell lines（BGC-823, SGC-7901, HGC-27, MGC-803, and NCI-N87）. pc-DNA3.1-FOXD3 or pc-DNA3.1 was transfected into SGC-7901 cells. Cell proliferation assay, clone formation assay, scratch healing assay, and Transwell chamber invasion assay were used to detected the effect of FOXD3 overexpression on the the proliferation, clone formation,migration, and invasion of SGC-7901 cells. The mRNA and protein expressions of epithelial-mesenchymal transition (EMT) related molecules before and after the transfection were detected by qRT-PCR and WB. Cell cycle changes before and after transfection were detected by Flow cytometry. Results: The expression of FOXD3 mRNA in GCA tissues was significantly downregulated, and it's expression was closely correlated with clinical stage and lymph node metastasis of GCA patients. The expression of FOXD3 in gastric cancer cell lines was lower than that in normal cell lines (all P<0.01). FOXD3 overexpression significantly inhibited the proliferation,clone formation, migration and invasion of SGC-7901 cells in vitro (all P<0.01). FOXD3 overexpression could up-regulate the expression of E-cadherin and down-regulate the expressions of N-cadherin, β -catenin and vimentin in SGC-7901 cells (all P<0.01). Overexpression of FOXD3 could arrest the cell cycle in the G0/G1 phase (P<0.01). Conclusion: The expression of FOXD3 in GCA tissues is significantly downregulated, and its overexpression can inhibit the biological behaviors of gastric cancer cells. FOXD3 can be used as a tumor suppressor gene to provide new ideas for tumor therapy.
2021, 28(8):818-823.
DOI: 10.3872/j.issn.1007-385X.2021.08.008
Abstract:
Objective: To explore the short-term efficacy and adverse reactions of bevacizumab combined with doxorubicin liposomes in the treatment of patients with platinum-resistant recurrent epithelial ovarian cancer, as well as the survival of patients. Methods: A total of 76 patients with platinum-resistant recurrent epithelial ovarian cancer who were admitted to the 901 Hospital of the People's Liberation Army (PLA) Joint Logistic Support Force from January 2018 to December 2019 were enrolled in this study. The patients were divided into a control group and an observation group with 38 cases in each by random number grouping method. The control group was given doxorubicin liposome single-agent chemotherapy for 4 cycles, while the observation group was given bevacizumab combined with doxorubicin liposome chemotherapy for 4 cycles. The short-term efficacy and adverse reactions of the two groups of patients after treatment were observed, and the changes in serum tumor markers HE4 (human epididymis protein 4) and CA125 (carbohydrate antigen 125) were detected. In addition, the patients were followed up for overall survival (OS) and disease progression[1]free survival (PFS). Results: The objective response rate (ORR) and disease control rate (DCR) of the control group were significantly lower than those of the observation group (ORR: 40.54% vs 69.44%; DCR: 67.57% vs 88.89%; all P<0.05). After treatment, the serum HE4 and CA125 levels of the observation group were (142.67±46.81) pmol/L and (31.79±11.65) U/L respectively, which were significantly lower than (219.33±75.67) pmol/L and (57.05±17.85) U/L of the control group (all P<0.05). There were no significant differences in adverse reactions such as gastrointestinal reactions, bone marrow suppression, liver and kidney damage, cardiotoxicity,allergic reactions, thromboembolism, and bleeding between the two groups (all P>0.05); the incidence of hypertension in the observation group was significantly higher than that in the control group (P<0.05), but it was controllable and tolerable. The median OS and median PFS of the patients in observation group were 17.2 months and 10.9 months respectively, which were significantly longer than the 14.1 months and 7.8 months of the control group (all P<0.05). Conclusion: For patients with platinum-resistant recurrent epithelial ovarian cancer, bevacizumab combined with doxorubicin liposomes has reliable short-term efficacy, good safety, and tolerable adverse reactions, which is worthy of clinical promotion.
Objective: To explore the short-term efficacy and adverse reactions of bevacizumab combined with doxorubicin liposomes in the treatment of patients with platinum-resistant recurrent epithelial ovarian cancer, as well as the survival of patients. Methods: A total of 76 patients with platinum-resistant recurrent epithelial ovarian cancer who were admitted to the 901 Hospital of the People's Liberation Army (PLA) Joint Logistic Support Force from January 2018 to December 2019 were enrolled in this study. The patients were divided into a control group and an observation group with 38 cases in each by random number grouping method. The control group was given doxorubicin liposome single-agent chemotherapy for 4 cycles, while the observation group was given bevacizumab combined with doxorubicin liposome chemotherapy for 4 cycles. The short-term efficacy and adverse reactions of the two groups of patients after treatment were observed, and the changes in serum tumor markers HE4 (human epididymis protein 4) and CA125 (carbohydrate antigen 125) were detected. In addition, the patients were followed up for overall survival (OS) and disease progression[1]free survival (PFS). Results: The objective response rate (ORR) and disease control rate (DCR) of the control group were significantly lower than those of the observation group (ORR: 40.54% vs 69.44%; DCR: 67.57% vs 88.89%; all P<0.05). After treatment, the serum HE4 and CA125 levels of the observation group were (142.67±46.81) pmol/L and (31.79±11.65) U/L respectively, which were significantly lower than (219.33±75.67) pmol/L and (57.05±17.85) U/L of the control group (all P<0.05). There were no significant differences in adverse reactions such as gastrointestinal reactions, bone marrow suppression, liver and kidney damage, cardiotoxicity,allergic reactions, thromboembolism, and bleeding between the two groups (all P>0.05); the incidence of hypertension in the observation group was significantly higher than that in the control group (P<0.05), but it was controllable and tolerable. The median OS and median PFS of the patients in observation group were 17.2 months and 10.9 months respectively, which were significantly longer than the 14.1 months and 7.8 months of the control group (all P<0.05). Conclusion: For patients with platinum-resistant recurrent epithelial ovarian cancer, bevacizumab combined with doxorubicin liposomes has reliable short-term efficacy, good safety, and tolerable adverse reactions, which is worthy of clinical promotion.
2021, 28(8):824-832.
DOI: 10.3872/j.issn.1007-385X.2021.08.009
Abstract:
Objective: To explore the expression level of microRNA-504 (miRNA-504) in gastric cancer (GC) tissues and its regulatory mechanism in the biological behaviors of GC cells. Methods: From June 2020 to December 2020, tumor tissues and corresponding para-cancerous tissues resected from 48 patients with gastric cancer were collected in the Department of Surgical, Sanya Central Hospital. qPCR was used to detect the mRNA levels of miR-504 and tumor protein 53-induced nuclear protein 1 (TP53INP1) in the tissues, and WB assay was used to detect the protein level of TP53INP1. Human gastric cancer BGC-823 cells were cultured in vitro and divided into control group (normally cultured BGC-823 cells), miR-504 mimic group, mimic-NC group, miR-504 inhibitor group,inhibitor-NC group, miR-504 inhibitor+si-NC group, and miR-504 inhibitor+si-TP53INP1 group. qRT-PCR was used to detect mRNA expression of miR-504 and TP53INP1 in each group of cells. MTT method, Flow cytometry, Scratch test, and Transwell invasion assay were used to detect the proliferation, apoptosis, migration, and invasion of the cells in each group. WB assay was used to detect the protein expression of cell proliferation, migration, and invasion-related proteins (Cyclin D1, E-cadherin, MMP-2, MMP-9) and TP53INP1 in each group. Dual-luciferase reporter gene experiment was used to further verify the targeting relationship between miR[1]504 and TP53INP1. Results: Compared with the para-cancerous tissues, the expression of miR-504 in gastric cancer tissues was significantly increased (P<0.05), and the mRNA and protein expression levels of TP53INP1 were significantly decreased (P<0.05 or P <0.01). The expression of miR-504 was negatively correlated with TP53INP1 mRNA (P<0.01). Compared with the control group, the expression of miR-504 in the BGC-823 cells of the miR-504 mimic group was significantly increased, while the mRNA and protein expression of TP53INP1 was significantly decreased (all P<0.05); moreover, the cell survival rate, scratch healing rate, the number of cells entering the lower layer of the Transwell chamber, and the expression of Cyclin D1, MMP-2, and MMP-9 were all significantly increased, while the apoptosis rate and the expression of E-cadherin were significantly decreased (all P<0.05) in miR-504 mimic group;However, the miR-504 inhibitor could significantly down-regulate the expression of miR-504, up-regulate the mRNA and protein expression of TP53INP1, inhibit cell proliferation, migration, and invasion, and promote cell apoptosis (all P<0.05) in BGC-823 cells.Down-regulating the expression of TP53INP1 could significantly reduce the inhibitory effect of down-regulation of miR-504 on the proliferation, migration, and invasion of BGC-823 cells; and miR-504 over-expression could obviously inhibit the luciferase activity of wild-type TP53INP1 plasmid (all P<0.05). Conclusion: miR-504 is highly expressed in gastric cancer tissues. Down-regulation of miR[1]504 can inhibit the malignant biological behaviors of gastric cancer BGC-823 cells and promote their apoptosis, and the mechanism may be related to the targeted regulation of the expression of TP53INP1.
Objective: To explore the expression level of microRNA-504 (miRNA-504) in gastric cancer (GC) tissues and its regulatory mechanism in the biological behaviors of GC cells. Methods: From June 2020 to December 2020, tumor tissues and corresponding para-cancerous tissues resected from 48 patients with gastric cancer were collected in the Department of Surgical, Sanya Central Hospital. qPCR was used to detect the mRNA levels of miR-504 and tumor protein 53-induced nuclear protein 1 (TP53INP1) in the tissues, and WB assay was used to detect the protein level of TP53INP1. Human gastric cancer BGC-823 cells were cultured in vitro and divided into control group (normally cultured BGC-823 cells), miR-504 mimic group, mimic-NC group, miR-504 inhibitor group,inhibitor-NC group, miR-504 inhibitor+si-NC group, and miR-504 inhibitor+si-TP53INP1 group. qRT-PCR was used to detect mRNA expression of miR-504 and TP53INP1 in each group of cells. MTT method, Flow cytometry, Scratch test, and Transwell invasion assay were used to detect the proliferation, apoptosis, migration, and invasion of the cells in each group. WB assay was used to detect the protein expression of cell proliferation, migration, and invasion-related proteins (Cyclin D1, E-cadherin, MMP-2, MMP-9) and TP53INP1 in each group. Dual-luciferase reporter gene experiment was used to further verify the targeting relationship between miR[1]504 and TP53INP1. Results: Compared with the para-cancerous tissues, the expression of miR-504 in gastric cancer tissues was significantly increased (P<0.05), and the mRNA and protein expression levels of TP53INP1 were significantly decreased (P<0.05 or P <0.01). The expression of miR-504 was negatively correlated with TP53INP1 mRNA (P<0.01). Compared with the control group, the expression of miR-504 in the BGC-823 cells of the miR-504 mimic group was significantly increased, while the mRNA and protein expression of TP53INP1 was significantly decreased (all P<0.05); moreover, the cell survival rate, scratch healing rate, the number of cells entering the lower layer of the Transwell chamber, and the expression of Cyclin D1, MMP-2, and MMP-9 were all significantly increased, while the apoptosis rate and the expression of E-cadherin were significantly decreased (all P<0.05) in miR-504 mimic group;However, the miR-504 inhibitor could significantly down-regulate the expression of miR-504, up-regulate the mRNA and protein expression of TP53INP1, inhibit cell proliferation, migration, and invasion, and promote cell apoptosis (all P<0.05) in BGC-823 cells.Down-regulating the expression of TP53INP1 could significantly reduce the inhibitory effect of down-regulation of miR-504 on the proliferation, migration, and invasion of BGC-823 cells; and miR-504 over-expression could obviously inhibit the luciferase activity of wild-type TP53INP1 plasmid (all P<0.05). Conclusion: miR-504 is highly expressed in gastric cancer tissues. Down-regulation of miR[1]504 can inhibit the malignant biological behaviors of gastric cancer BGC-823 cells and promote their apoptosis, and the mechanism may be related to the targeted regulation of the expression of TP53INP1.
2021, 28(8):833-838.
DOI: 10.3872/j.issn.1007-385X.2021.08.010
Abstract:
乙型肝炎病毒（HBV）慢性感染是诱发肝细胞癌（HCC）的重要危险因素，而炎症的持续存在可形成一种适宜肿瘤存活 的微环境（TME），其X基因编码并表达的乙型肝炎病毒X蛋白（HbX）作为一个多功能调节蛋白，它通过与TME中的肿瘤细胞及 周围基质成分相互作用，促进HCC的发生和发展。本文通过对近期文献进行回顾总结，着重分析了HbX在HCC-TME中引发 HCC侵袭和转移的作用机制，包括参与癌细胞增殖与凋亡、抑制机体免疫、促进肝细胞自噬、诱导细胞外基质重塑以及调控干细 胞特性等方面，以期为临床HBV相关HCC提供新的治疗思路。
乙型肝炎病毒（HBV）慢性感染是诱发肝细胞癌（HCC）的重要危险因素，而炎症的持续存在可形成一种适宜肿瘤存活 的微环境（TME），其X基因编码并表达的乙型肝炎病毒X蛋白（HbX）作为一个多功能调节蛋白，它通过与TME中的肿瘤细胞及 周围基质成分相互作用，促进HCC的发生和发展。本文通过对近期文献进行回顾总结，着重分析了HbX在HCC-TME中引发 HCC侵袭和转移的作用机制，包括参与癌细胞增殖与凋亡、抑制机体免疫、促进肝细胞自噬、诱导细胞外基质重塑以及调控干细 胞特性等方面，以期为临床HBV相关HCC提供新的治疗思路。
2021, 28(8):839-843.
DOI: 10.3872/j.issn.1007-385X.2021.08.011
Abstract:
靶向治疗和免疫治疗在NSCLC治疗中发挥了重要作用。TKI可以显著延长EGFR突变患者的生存时间，然而对于发 生TKI耐药患者的有效治疗方法有限，仍需要探索除化疗外的其他治疗手段。虽然免疫治疗能够改善NSCLC患者的无进展生 存期和总生存期，但既往数据表明，EGFR突变NSCLC患者接受免疫治疗的效果仍不理想。本文综述了EGFR突变NSCLC患者 肿瘤微环境特点及其与免疫治疗之间的关系，并探讨未来如何优化免疫治疗在这部分人群中的应用。
靶向治疗和免疫治疗在NSCLC治疗中发挥了重要作用。TKI可以显著延长EGFR突变患者的生存时间，然而对于发 生TKI耐药患者的有效治疗方法有限，仍需要探索除化疗外的其他治疗手段。虽然免疫治疗能够改善NSCLC患者的无进展生 存期和总生存期，但既往数据表明，EGFR突变NSCLC患者接受免疫治疗的效果仍不理想。本文综述了EGFR突变NSCLC患者 肿瘤微环境特点及其与免疫治疗之间的关系，并探讨未来如何优化免疫治疗在这部分人群中的应用。
2021, 28(8):844-849.
DOI: 10.3872/j.issn.1007-385X.2021.08.012
Abstract:
PD-1/PD-L1抑制剂作为免疫检查点抑制剂已经改变了多种肿瘤治疗的现状。在三阴性乳腺癌（triple-negative breast cancer，TNBC）中，以阿替利珠单抗和帕博利珠单抗为代表的PD-1/PD-L1抑制剂已经成为晚期患者一线治疗、早期患者新辅助治 疗的标准方案；其是否用于术后高危分型的辅助治疗，目前尚无结论。本文就目前PD-1/PD-L1抑制剂在TNBC中治疗的现状及 应用前景的相关进展进行综述。
PD-1/PD-L1抑制剂作为免疫检查点抑制剂已经改变了多种肿瘤治疗的现状。在三阴性乳腺癌（triple-negative breast cancer，TNBC）中，以阿替利珠单抗和帕博利珠单抗为代表的PD-1/PD-L1抑制剂已经成为晚期患者一线治疗、早期患者新辅助治 疗的标准方案；其是否用于术后高危分型的辅助治疗，目前尚无结论。本文就目前PD-1/PD-L1抑制剂在TNBC中治疗的现状及 应用前景的相关进展进行综述。
2021, 28(8):850-857.
DOI: 10.3872/j.issn.1007-385X.2021.08.013
Abstract:
唾液酸结合免疫球蛋白样凝集素（sialic acid-binding immunoglobulin-type lectin，Siglec）是一类能够识别唾液酸化聚 糖结构的膜蛋白，近年来，随着对Siglec调节肿瘤微环境研究的深入，其已成为抗肿瘤药物研发的重要方向之一。本文系统介绍 Siglec家族成员中的Siglec-1、-2、-3、-7、-9、-10、-15通过与其各自配体相互作用而调节固有免疫或适应性免疫的机制及其在抗肿 瘤治疗中的应用进展，为肿瘤免疫治疗提供新的思路。
唾液酸结合免疫球蛋白样凝集素（sialic acid-binding immunoglobulin-type lectin，Siglec）是一类能够识别唾液酸化聚 糖结构的膜蛋白，近年来，随着对Siglec调节肿瘤微环境研究的深入，其已成为抗肿瘤药物研发的重要方向之一。本文系统介绍 Siglec家族成员中的Siglec-1、-2、-3、-7、-9、-10、-15通过与其各自配体相互作用而调节固有免疫或适应性免疫的机制及其在抗肿 瘤治疗中的应用进展，为肿瘤免疫治疗提供新的思路。
联系方式
- 《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
您是第位访问者
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.