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作 者:姚田 马文娟 YAO Tian;MA Wenjuan(Department of Obstetrics and Gynecology,Xi’an People’s Hospital,Xi’an 710004,China)
机构地区:[1]西安市人民医院西安市第四医院妇产科,陕西西安710004
出 处:《陕西医学杂志》2023年第4期390-394,共5页Shaanxi Medical Journal
基 金:西安市人民医院(西安市第四医院)科研孵化基金资助项目(FZ-55)。
摘 要:目的:研究RP11-444D3.1与SOX5基因共表达对子宫内膜癌细胞Ishikawa侵袭的影响,并探究其分子机制。方法:通过过表达RP11-444D3.1和SOX5基因的腺病毒转染子宫内膜癌细胞Ishikawa,构建过表达RP11-444D3.1和SOX5基因及共表达RP11-444D3.1、SOX5基因的子宫内膜癌细胞,通过实时定量PCR(qRT-PCR)检测细胞中RP11-444D3.1和SOX5基因mRNA表达水平,通过划痕实验和Transwell实验检测过表达RP11-444D3.1和SOX5基因的子宫内膜癌细胞的侵袭能力,并通过Western blot法检测cofilin/LIMK/Rac信号通路蛋白的相对表达量。结果:与子宫内膜癌细胞Ishikawa相比,过表达RP11-444D3.1与SOX5基因及共表达RP11-444D3.1、SOX5基因的子宫内膜癌细胞具有更强的侵袭能力(均P<0.05),同时,cofilin蛋白的表达降低,LIMK/Rac蛋白的磷酸化水平上调。结论:RP11-444D3.1与SOX5基因均可激活cofilin/LIMK/Rac信号通路,共表达可增强对cofilin/LIMK/Rac信号通路的激活作用,介导子宫内膜癌细胞侵袭。Objective:To study the effect of co-expression of RP11-444D3.1 and SOX5 gene on the invasion of endometrial carcinoma cell line Ishikawa,and explore its molecular mechanism.Methods:Endometrial cancer cells Ishikawa were transfected with adenoviruses overexpressing RP11-444D3.1 and SOX5 genes,and endometrial cancer cells overexpressing RP11-444D3.1 and SOX5 genes and co-expressing RP11-444D3.1 and SOX5 genes were constructed.The mRNA expression levels of RP11-444D3.1 and SOX5 genes in the cells were detected by real-time quantitative PCR(qRT-PCR),and the invasive ability of endometrial cancer cells overexpressing RP11-444D3.1 and SOX5 genes was detected by scratch test and Transwell test,and the relative expression of cofilin/LIMK/RAC signal pathway protein was detected by Western Blot method.Results:Compared with Ishikawa,endometrial cancer cells overexpressing RP11-444D3.1 and SOX5 genes and co-expressing RP11-444D3.1 and SOX5 genes had stronger invasive ability.At the same time,the expression of cofilin protein decreased,and the phosphorylation level of LIMK/RAC protein increased.Conclusion:Both RP11-444D3.1 and SOX5 genes can activate the cofilin/LIMK/Rac signal pathway,and co-expression can enhance the activation of cofilin/LIMK/Rec signal pathway and mediate the invasion of endometrial cancer cells.
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