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作 者:严智文 张亮[1] 王春雨[1] 陈怀龙 YAN Zhi-wen;ZHANG Liang;WANG Chun-yu;CHEN Huai-long(Department of Anesthesiology,Qingdao Eighth People's Hospital,Qingdao 266000,China)
机构地区:[1]山东省青岛市第八人民医院麻醉科,青岛266000
出 处:《微循环学杂志》2023年第3期1-5,11,共6页Chinese Journal of Microcirculation
基 金:山东省医学会舒适化医疗专项资金(YXH2021ZX011)。
摘 要:目的:探讨瑞马唑仑(REM)对胃癌细胞增殖、迁移和侵袭的影响及可能机制。方法:体外培养人胃癌细胞系SGC7901,分为对照组、REM低(80μM)、中(160μM)、高(320μM)浓度组(REM-L、M、H组)和REM(320μM)+Wnt/β-catenin信号通路激活剂氯化锂(LiCl,20mM)组(REM+LiCl组),采用MTT法、克隆形成实验分别检测各组SGC7901细胞增殖活力和克隆形成能力,Transwell实验检测各组SGC7901细胞迁移、侵袭能力,Western Blotting检测各组SGC7901细胞中Wnt1、β-catenin、c-Myc、Cyclin D1、MMP-2、MMP-9蛋白表达。结果:与对照组比较,REM-L、M、H组SGC7901细胞增殖活力、克隆形成能力、迁移和侵袭能力及细胞中c-Myc、Cyclin D1、MMP-2、MMP-9、Wnt1、β-catenin蛋白表达水平显著降低(P<0.01);而与REM-H组比较,REM+LiCl组SGC7901细胞上述指标显著升高(P<0.01)。结论:REM可抑制胃癌细胞增殖、迁移和侵袭,其作用机制可能与其抑制Wnt/β-catenin信号通路激活有关。Objective:To investigate the effects of remimazolan(REM)on the proliferation,migration and invasion of gastric cancer cells and its possible mechanism.Method:Human gastric cancer cell line SGC7901 was cultured in vitro and divided into control group,low(80μM),medium(160μM)and high(320μM)REM concentration group(REM-L,M and H groups)and REM(320μM)+Wnt/β-catenin signaling pathway activator LiCl(20 mM)group(REM+LiCl group).The proliferation activity and clonogenesis ability of SGC7901 cells in each group were detected by MTT assay and clonal formation assay.The migration and invasion ability of SGC7901 cells in each group were detected by Transwell assay.The expressions of Wnt1,β-catenin,c-Myc,Cyclin D1,MMP-2 and MMP-9 in SGC7901 cells of each group were detected by Western blot.Results:Compared with the control group,the proliferative activity,clonal formation ability,migration and invasion ability of SGC7901 cells and the protein expression levels of c-Myc,Cyclin D1,MMP-2,MMP-9,Wnt1 andβ-catenin in REM-L,M and H groups were significantly decreased(P<0.01),while compared with REM-H group,these indexes in REM+LiCl group were significantly increased(P<0.01).Conclusion:REM can inhibit the proliferation,migration and invasion of gastric cancer cells,and its mechanism may be related to inhibiting the activation of Wnt/β-catenin signal pathway.
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