miR-506 Regulates Epithelial Mesenchymal Transition in Breast Cancer Cell Lines

被引：96

作者：

Arora, Himanshu ^{[1
]}

Qureshi, Rehana ^{[1
]}

Park, Woong-Yang ^{[2
,3
]}

机构：

[1] Seoul Natl Univ, Coll Med, Dept Biomed Sci, Seoul, South Korea

[2] Sungkyunkwan Univ, Sch Med, Dept Mol Cell Biol, Seoul, South Korea

[3] Sungkyunkwan Univ, Sch Med, Samsung Med Ctr, Samsung Genome Inst, Seoul, South Korea

来源：

PLOS ONE | 2013年 / 8卷 / 05期

基金：

新加坡国家研究基金会;

关键词：

NF-KAPPA-B; KINASE ACTIVATION; TETRASPANIN CD151; PROSTATE-CANCER; STEM-CELLS; PROGRESSION; GROWTH; PROLIFERATION; EXPRESSION; MIGRATION;

D O I：

10.1371/journal.pone.0064273

中图分类号：

O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];

学科分类号：

070301 [无机化学]; 070403 [天体物理学]; 070507 [自然资源与国土空间规划学]; 090105 [作物生产系统与生态工程];

摘要：

Epithelial-mesenchymal transition (EMT) is an important parameter related to breast cancer survival. Among several microRNAs predicted to target EMT-related genes, miR-506 is a novel miRNA found to be significantly related to breast cancer patient survival in a meta-analysis. miR-506 suppressed the expression of mesenchymal genes such as Vimentin, Snai2, and CD151 in MDA-MB-231 human breast cancer cell line. Moreover, NF-kappa B bound to the upstream promoter region of miR-506 to suppress transcription. Overexpression of miR-506 inhibited TGF beta-induced EMT and suppressed adhesion, invasion, and migration of MDA-MB-231 cells. From these results, we concluded that miR-506 plays a key role in the process of EMT through posttranslational control of EMT-related genes.

引用

页数：7

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