%0 Journal Article
%T miR-198靶向MAPK1调控宫颈癌HeLa细胞增殖、凋亡和侵袭
%A 张秀玲
%A 朱利红
%A 李少儒
%A 段树鹏
%A 王世进
%A 秦海霞
%A 赵淑珍
%J 肿瘤防治研究
%D 2018
%R 10.3971/j.issn.1000-8578.2018.18.0537
%X 摘要 目的 探究miR-198对宫颈癌细胞增殖、凋亡和侵袭的作用及其机制。方法 用miR-198 mimic转染HeLa细胞，qRT-PCR检测miR-198和丝裂原活化蛋白激酶1 （Mitogen-activated protein kinase1, MAPK1）的mRNA水平；荧光素酶实验检测miR-198和MAPK1的靶向关系；用pcDNA3.0-MAPK1（pc-MAPK1）和miR-198 mimic转染细胞，CCK-8检测细胞增殖活性，流式细胞术检测细胞凋亡，Transwell法检测细胞侵袭能力，Western blot检测蛋白的表达。结果 miR-198 mimic转染细胞后，miR-198表达水平明显升高，MAPK1 mRNA表达水平明显降低；荧光素酶报告实验表明miR-198序列上存在MAPK1结合位点；miR-198过表达能显著降低宫颈癌细胞增殖倍数、诱导细胞凋亡，同时还能明显降低HeLa细胞侵袭能力；此外，miR-198 mimic能显著抑制MAPK1下游基因核糖体S6激酶2（Ribosomal S6 kinase 2, RSK2）、c-Myc和c-fos的蛋白表达；pc-MAPK1能明显减弱miR-198 mimic对HeLa细胞增殖、凋亡、侵袭及对MAPK1下游蛋白表达的调控作用。结论 miR-198过表达能通过靶向MAPK1抑制宫颈癌细胞的增殖和侵袭能力并诱导细胞凋亡
%K 宫颈癌
%K miR-198
%K MAPK1
%K 凋亡
%K 侵袭
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%U http://www.zlfzyj.com/CN/abstract/abstract9291.shtml