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CLIC1对氯化钴诱导的胃癌细胞增殖侵袭及MAPK/ERK通路的影响 预览

Effects of CLIC1 on Proliferation, Invasion and MAPK/ERK Pathway of Cobalt Chloride-induced Gastric Cancer Cells
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摘要 目的:探讨CLIC1对氯化钴诱导的胃癌细胞增殖、侵袭及MAPK/ERK通路的影响。方法:体外培养胃癌细胞SGC-7901后分为4组,正常组(control组)、氯化钴处理组(150umCoCl2处理);阴性转染组(si-NC组,CoCl2处理后继续培养48h,转染NCsiRNA);CLIC1干扰组(si-CLIC1组,CoCl2处理后继续培养48h,转染CLIC1siRNA)。收集细胞上清,MTT法检测SGC-7901细胞活力;平板细胞克隆形成实验检测菌落形成;划痕实验检测细胞转移能力;Transwell小室检测细胞迁移、侵袭能力;蛋白免疫印迹(WB)检测MAPK/ERK通路有关蛋白的表达。结果:与control组相比,CoCl两组、si-NC组细胞抑制率、转移抑制率、E-cadherin蛋白表达均升高,菌落数量、迁移、侵袭数量均降低,p-ERK1/2、MMP-9、N-cadherin蛋白表达降低(P<0.05),抑制CLIC1表达后细胞抑制率、转移抑制率、E-cadherin蛋白表达进一步升高,菌落数量、迁移、侵袭数量以及p-ERK1/2、MMP-9、N-cadherin蛋白表达进一步降低(P<0.05)。结论:CoCl2处理后可抑制胃癌细胞的增殖、侵袭,而抑制CLIC1表达后能够协同CoCl2进一步抑制胃癌细胞的增殖、侵袭,这可能与抑制MAPK/ERK通路有关。 Objective:To study the effects of CLIC1 on the proliferation,invasion and MAPK/ERK pathway of gastric cancer cells induced by cobalt chloride,so as to provide certain ideas for the treatment of diseases.Methods:After cultured gastric cancer cells SGC-7901 in vitro,they were divided into 4 groups,the normal group(group control)and the cobalt chloride treatment group(150um CoCl2 treatment); in the negative transfection group(group si-NC,CoCl2 was treated with 48h and transfected with NC siRNA); CLIC1 interference group(group si-CLIC1,CoCl2 after treatment continued to cultivate 48h,transfected CLIC1siRNA).The cell supernatants were collected,the viability of SGC-7901 cells was detected by MTT; colony formation assay was used to detect colony formation; the scratch test was used to detect the cell transfer ability; transwell cell was used to detect cell migration and invasion; Western blot(WB)was used to detect the expression of MAPK/ERK pathway related proteins.Results:Compared with control group,the inhibition rate,metastasis inhibition rate and E-cadherin protein expression in CoCl2 group and si-NC group increased,the number of colonies,migration and invasion decreased,while the expression of p-ERK1/2,MMP-9 and N-cadherin protein decreased(P<0.05).After inhibiting CLIC1 expression,the inhibition rate,metastasis inhibition rate and E-cadherin protein expression increased further,and the number,migration and invasion of colonies increased.The number and expression of p-ERK1/2,MMP-9 and N-cadherin protein were further decreased(P<0.05).Conclusion:CoCl2 treatment can inhibit the proliferation and invasion of gastric cancer cells,and the inhibition of CLIC1 expression can further inhibit the proliferation and invasion of gastric cancer cells in coordination with CoCl2,which may be related to the inhibition of MAPK/ERK pathway.
作者 王志强 孙鹏 高淳 徐铭 张云鹏 程大庆 王珏 WANG Zhiqiang;SUN Peng;GAO Chun(Shanghai Tongren Hospital,Shanghai 200336,China)
出处 《河北医学》 CAS 2019年第1期99-104,共6页 Hebei Medicine
基金 上海市长宁区科学技术委员会计划项目,(编号:CNKW2015Y02)。
关键词 胃癌 氯化钴 CLIC1 Gastric cancer Cobalt chloride CLIC1
作者简介 通讯作者:王珏
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