MiR-199b-5p targets HER2 in breast cancer cells

被引：72

作者：

Fang, Chen ^{[1
]}

Zhao, Yu ^{[2
]}

Guo, Baoyu ^{[1
]}

机构：

[1] Second Mil Med Univ, Dept Biochem Pharm, Sch Pharm, Shanghai 200433, Peoples R China

[2] Shanghai Jiao Tong Univ, Sch Med, Shanghai Key Lab Gastr Neoplasms, Dept Surg,Shanghai Inst Digest Surg,Ruijin Hosp, Shanghai 200025, Peoples R China

来源：

JOURNAL OF CELLULAR BIOCHEMISTRY | 2013年 / 114卷 / 07期

基金：

中国国家自然科学基金;

关键词：

HER2; microRNA; miR-199b-5p; BREAST CANCER; LAPATINIB RESISTANCE; EXPRESSION; MICRORNA; RECEPTOR; ERBB2; ACTIVATION; PROTEIN; METASTASIS; INHIBITOR; MECHANISM;

D O I：

10.1002/jcb.24487

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

HER2 (ErbB2) has been reported to be overexpressed in 2030% of breast cancer and confers poor survival because of high proliferation and metastasis rates. MicroRNAs are small noncoding RNAs that are responsible for the post-transcriptional regulation of target genes. We found miR-199b-5p inhibited HER2 expression by direct targeting its 3-untranslated region (3UTR) in breast cancer cells. In addition, miR-199b-5p inhibited HER2 downstream signaling by ERK1/2 and AKT pathways in breast cancer cells. Besides, transwell migration, wound healing, and clonogenicity were obviously inhibited by overexpression of miR-199b-5p in HER2-positive breast cancer cells. We also found that miR-199b-5p could enhance the suppression of trastuzumab on cell migration and clonogenicity. These results suggest that miR-199b-5p may have the potential to be a novel important alternative therapeutic target for HER2-positive breast cancer. J. Cell. Biochem. 114: 14571463, 2013. (c) 2013 Wiley Periodicals, Inc.

引用

页码：1457 / 1463

页数：7

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