MiR-101 inhibits melanoma cell invasion and proliferation by targeting MITF and EZH2

被引：66

作者：

Luo, Chonglin ^{[1
]}

Merz, Patrick R. ^{[1
]}

Chen, Yiwei ^{[2
]}

Dickes, Elke ^{[1
]}

Pscherer, Armin ^{[3
]}

Schadendorf, Dirk ^{[4
,5
]}

Eichmueller, Stefan B. ^{[1
,4
]}

机构：

[1] German Canc Res Ctr, Dept Translat Immunol, Heidelberg, Germany

[2] Max Planck Inst Med Res, Dept Mol Neurobiol, D-69120 Heidelberg 1, Germany

[3] BioRN Cluster Management GmbH, Heidelberg, Germany

[4] German Canc Consortium DKTK, Heidelberg, Germany

[5] Univ Duisburg Essen, Univ Hosp Essen, West German Canc Ctr, Dept Dermatol, Essen, Germany

来源：

CANCER LETTERS | 2013年 / 341卷 / 02期

关键词：

MicroRNA; Melanoma; Invasion; Microphthalmia-associated transcription factor; Enhancer of zeste homolog 2; MICRORNA EXPRESSION LEVELS; GROUP PROTEIN EZH2; MALIGNANT-MELANOMA; HEPATOCELLULAR-CARCINOMA; INDEPENDENT GROWTH; DOWN-REGULATION; CANCER-CELLS; LUNG-CANCER; GENES; LINES;

D O I：

10.1016/j.canlet.2013.08.021

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

The microRNA miR-101 has been reported to be a tumor suppressor. Here we show that low expression of miR-101 is associated with poor survival in stage IV melanoma patients. We identified microphthalmia-associated transcription factor (MITF) as a direct target of miR-101. In melanoma cells, overexpression of miR-101 downregulated protein levels of MITF and a previously reported target protein, enhancer of zeste homolog 2 (EZH2). Functional assays showed that miR-101 suppressed invasion and proliferation - an outcome that could be phenocopied by siRNA knockdown of MITF and EZH2. Our data suggest that miR-101 might have a beneficial role in melanoma. (C) 2013 Elsevier Ireland Ltd. All rights reserved.

引用

页码：240 / 247

页数：8

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