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miRNA-101-3 p inhibits proliferation and migration of gastric cancer cells by targeting EZH2 / 中国病理生理杂志
Chinese Journal of Pathophysiology ; (12): 2143-2150, 2017.
Article de Zh | WPRIM | ID: wpr-663239
Bibliothèque responsable: WPRO
ABSTRACT
AIM:To investigate the role of microRNA-101-3p (miRNA-101-3p) on the proliferation, apopto-sis and invasion of gastric cancer cells and the possible regulatory mechanisms .METHODS: The expression of miRNA-101-3p in two kinds of gastric cancer cells and a gastric mucosal cell line was detected by real -time PCR.The miRNA-101-3p was overexpressed by Lipofectamine 2000 transfection with miRNA-101-3p mimics.The effects of miRNA-101-3p on cell cycle distribution and apoptosis were analyzed by flow cytometry .The effects of miRNA-101-3p on cell proliferation and migration abilities were detected by CCK-8 assay, trypan blue exclusion test and Transwell assay .The protein expression of enhancer of zeste homolog 2 ( EZH2) was determined by Western blot .RESULTS: The expression of miRNA-101-3p in gastric cancer cells was lower than that in gastric mucosal cells (P<0.05).The gastric cancer cell MGC-803 had the low-est expression level of miRNA-101-3p.The result of flow cytometry showed that the population of S phase was reduced , and the population of G0/G1 phase and the early stage apoptotic rate were increased after the expression of miRNA-101-3p was overexpressed (P<0.05).The results of CCK-8 assay, trypan blue exclusion test and Transwell assay showed that overex-pression of miRNA-101-3p significantly reduced the proliferation and migration abilities of gastric cancer cells (P<0.05). Overexpression of miRNA-101-3p decreased the protein level of EZH2 (P<0.05).CONCLUSION:miRNA-101-3p may suppresses the gastric cancer cell proliferation and migration , and promotes the gastric cancer cell apotosis by down-regula-tion of EZH2.
Mots clés
Texte intégral: 1 Base de données: WPRIM Langue: Zh Journal: Chinese Journal of Pathophysiology Année: 2017 Type de document: Article
Texte intégral: 1 Base de données: WPRIM Langue: Zh Journal: Chinese Journal of Pathophysiology Année: 2017 Type de document: Article