miR-7-5p靶向抑制REGγ对三阴性乳腺癌细胞MDA-MB-231迁移及侵袭能力的调控作用

Effect of miR-7-5p inhibiting migration and invasion of triple-negative breast cancer cells MDA-MB-231 by regulating REGγ

目的:探讨miR-7-5p靶向抑制REGγ对三阴性乳腺癌细胞MDA-MB-231迁移和侵袭能力的调控作用。方法:培养乳腺癌MDA-MB-231细胞,设置阴性对照组、REGγ敲减组、miR-7-5p过表达组、miR-7-5p+REGγ同时过表达组。采用划痕愈合实验检测细胞的迁移能力;Transwell实验检测细胞的侵袭能力;qRT-PCR检测REGγ和miR-7-5p的表达水平;荧光素酶报告基因检测miR-7-5p靶向调控REGγ。结果:miR-7-5p可特异结合REGγ的3端非翻译区。与阴性对照组相比,敲减REGγ可抑制MDA-MB-231细胞的迁移及侵袭能力(P<0.05);过表达miR-7-5p可降低REGγ的表达水平(P<0.05),并抑制MDA-MB-231细胞的迁移及侵袭能力(P<0.05)。与过表达miR-7-5p相比,同时过表达miR-7-5p和REGγ可降低miR-7-5p对MDA-MB-231细胞迁移和侵袭能力的抑制作用(P<0.05)。结论:miR-7-5p能够抑制三阴性乳腺癌细胞MDA-MB-231的迁移和侵袭能力,机制可能与靶向调控REGγ的表达水平有关。

Objective:To explored the effect of miR-7-5p inhibiting migration and invasion of triple-negative breast cancer cells MDA-MB-231 by regulating REGγ.Methods:Triple-negative breast cancer cells MDA-MB-231 were cultured and grouped,which included negative control group,REGγinhibiting group,miR-7-5p over-expressing group,miR-7-5p and REGγco-expressing group.Wound healing assay was used to measure cell migration,transwell assay was used to measure cell invasion,qRT-PCR was used to detect the expression of REGγand miR-7-5p,luciferase reporter assay was used to verify the relationship between miR-7-5p and REGγ.Results:miR-7-5p could bind the 3 untranslated regions of REGγdirectly in MDA-MB-231 cells.Compared with negative control group,knockdown of REGγcould inhibit the migration and invasion of MDA-MB-231 cells(P<0.05).The overexpression of miR-7-5p reduced the expression level of REGγ(P<0.05),and inhibit the migration and invasion of MDA-MB-231 cells.Compared with the overexpression of miR-7-5p,simultaneous overexpression of miR-7-5p and REGγreduced the inhibitory effect of miR-7-5p on the migration and invasion of MDA-MB-231 cells Conclusion:miR-7-5p suppressed cell migration and invasion in MDA-MB-231 cells,and mainly by targeting REGγ.miR-7-5p can inhibit the migration and invasion of triple negative breast cancer cell line MDA-MB-231,the mechanism may be related to the targeted regulation of REGγ.