| Literature DB >> 24508260 |
Jing Fu1, Xiaojie Xu2, Lei Kang3, Liying Zhou2, Shibin Wang4, Juming Lu5, Long Cheng2, Zhongyi Fan2, Bin Yuan2, Peirong Tian5, Xiaofei Zheng6, Chengze Yu7, Qinong Ye8, Zhaohui Lv9.
Abstract
Eye absent (Eya) proteins are involved in cell fate determination in a broad spectrum of cells and tissues. Aberrant expression of Eya2 has been documented in a variety of cancers and correlates with clinical outcome. However, whether microRNAs (miRNAs) can regulate Eya2 expression remains unknown. Here, we show that miR-30a represses Eya2 expression by binding to the 3'-untranslated region of Eya2. Overexpression of Eya2 in miR-30a-transfected breast cancer cells effectively rescued the inhibition of cell proliferation and migration caused by miR-30a. Knockdown of Eya2 by small-interfering RNA (siRNA) in breast cancer cells mimicked the effect induced by miR-30a and abolished the ability of miR-30a to regulate breast cancer cell proliferation and migration. The miR-30a/Eya2 axis could regulate G1/S cell cycle progression, accompanied by the modulation of expression of cell cycle-related proteins, including cyclin A, cyclin D1, cyclin E, and c-Myc. Moreover, miR-30a expression was downregulated in breast cancer patients, and negatively correlated with Eya2, which was upregulated in breast cancer patients. These data suggest that the miR-30a/Eya2 axis may play an important role in breast cancer development and progression and that miR-30a activation or Eya2 inhibition may be a useful strategy for cancer treatment.Entities:
Keywords: Breast cancer; Cell migration; Cell proliferation; Eya2; miR-30a
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Year: 2014 PMID: 24508260 DOI: 10.1016/j.bbrc.2014.01.174
Source DB: PubMed Journal: Biochem Biophys Res Commun ISSN: 0006-291X Impact factor: 3.575