摘要
目的:探讨胱硫醚-β-合酶(CBS)和胱硫醚-γ-裂解酶(CSE)的表达及其对乳腺癌细胞恶性生物学行为的影响,并阐明其作用机制。方法:选择15例乳腺癌患者的乳腺癌组织和癌旁正常组织,采用实时荧光定量PCR(RT-qPCR)和Western blotting法检测乳腺癌组织和癌旁正常组织以及MCF-7细胞和MDA-MB-231细胞中CBS和CSE的mRNA及蛋白表达水平。将MCF-7细胞分为siNC组(转染siNC)和siCBS组(转染siCBS),MDA-MB-231细胞分为ovNC组(转染CSE过表达空载质粒)和ovCSE组(转染CSE过表达质粒)。CCK-8法检测各组乳腺癌细胞的增殖活性,Transwell小室实验检测各组细胞的迁移和侵袭细胞数,Western blotting法检测各组乳腺癌细胞中E钙黏蛋白(E-cadherin)、神经钙黏蛋白(N-cadherin)和波形蛋白(Vimentin)表达水平。结果:与癌旁正常组织比较,乳腺癌组织中CBS和CSE mRNA及蛋白表达水平升高(P<0.05或P<0.01)。与MDA-MB-231细胞比较,MCF-7细胞中CBS mRNA表达水平升高(P<0.05);与MCF-7细胞比较,MDA-MB-231细胞中CSE蛋白表达水平降低(P<0.05)。与siNC组比较,siCBS组MCF-7细胞增殖活性、迁移和侵袭细胞数、N-cadherin和Vimentin蛋白表达水平明显降低(P<0.05),E-cadherin蛋白表达水平明显升高(P<0.05)。与ovNC组比较,ovCSE组MDA-MB-231细胞增殖活性、迁移和侵袭细胞数、N-cadherin和Vimentin蛋白表达水平明显升高(P<0.05),E-cadherin蛋白表达水平明显降低(P<0.05)。结论:CBS和CSE在乳腺癌组织中表达上调,高水平的CBS和CSE促进乳腺癌细胞的增殖、迁移、侵袭和上皮-间质转化(EMT)。
Objective:To investigate the expressions of cystathionine-β-synthase(CBS)and cystathionine-γ-lyase(CSE)and their effects on the malignant biological behaviours of breast cancer cells,and to elucidate their mechanisms.Methods:The breast cancer tissue and paracancerous normal tissue from 15 cases of patients were selected,and RT-qPCR and Western blotting methods were used to detect the mRNA and protein expression levels of CBS and CSE in breast cancer tissue,paracancerous normal tissue,MCF-7 cells,and MDA-MB-231 cells.The MCF-7 cells were divided into siNC group(transfected with siNC)and siCBS group(transfected with siCBS),and the MDA-MB-231 cells were divided into ovNC group(transfected with CSE over-expression empty plasmid)and ovCSE group(transfected with CSE over-expression plasmid).CCK8 assay was used to detect the proliferation activities of breast cancer cells in various groups,Transwell assay was used to detect the numbers of migration and invasion cells in various groups,and Western blotting method was used to detect the protein expression levels of E-cadherin,N-cadherin and Vimentin proteins in the breast cancer cells in various groups.Results:Compared with paracancerous normal tissue,the expression levels of CBS and CSE mRNA and proteins in breast cancer tissue were increased(P<0.05 or P<0.01).Compared with MDA-MB-231 cells,the CBS mRNA expression level in the MCF-7 cells was increased(P<0.05);compared with MCF-7 cells,the expression level of CSE protein in the MDA-MB-231 cells was decreased(P<0.05).Compared with siNC group,the proliferation activity,the numbers of migration and invasion cells,the expression levels of N-cadherin and Vimentin proteins in the MCF-7 cells in siCBS group were significantly decreased(P<0.05),and the expression level of E-cadherin protein was increased(P<0.05).Compared with ovNC group,the proliferation activity,the numbers of migratoin and invasion cells,and the expression levels of N-cadherin and Vimentin proteins in the MDA-MB-231 cells in ovCSE group were increased(P<0.05),while the expression level of E-cadherin protein was significantly decreased(P<0.05).Conclusion:The expressions of CBS and CSE are upregulated in breast cancer tissue,and high levels of CBS and CSE promote proliferation,migration,invasion and epithelial-mesenchymal transition(EMT)of breast cancer cells.
作者
赵蒙蒙
王雅璐
许宇翔
杨凯歌
曹玉文
周文虎
费晶
王雯
罗成华
胡建明
ZHAO Mengmeng;WANG Yalu;XU Yuxiang;YANG Kaige;CAO Yuwen;ZHOU Wenhu;FEI Jing;WANG Wen;LUO Chenghua;HU Jianming(Department of Pathology,School of Medicine,Shihezi University,Department of Pathology,First Affiliated Hospital,Shihezi University,Shiheizi 832002,China;Department of Oncology,First Affiliated Hospital,Shihezi University,Shiheizi 832002,China;Department of Pharmacy,Xiangya School of Pharmaceutical Sciences,Central South University,Changsha 410013,China;Department of Physiology and Pathophysiology,School of Basic Medicine,Capital Medical University,Beijing 100069,China)
出处
《吉林大学学报(医学版)》
北大核心
2025年第1期34-43,共10页
Journal of Jilin University:Medicine Edition
基金
国家自然科学基金项目(82103290)
新疆维吾尔自治区人力资源和社会保障厅“天池英才”计划项目(CZ003103)
新疆生产建设兵团科技研究指导项目(2022ZD003,2023ZD029)
新疆生产建设兵团科技计划项目(2024DA041)
石河子大学国家大学生创新创业训练计划项目(202410759083)
石河子大学青年创新拔尖人才项目(CXBJ202207)
新疆生产建设兵团重点领域科技攻关项目(2023AB0S8)。
