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Biochem Biophys Res Commun. 2014 Mar 7;445(2):314-9. doi: 10.1016/j.bbrc.2014.01.174. Epub 2014 Feb 4.

miR-30a suppresses breast cancer cell proliferation and migration by targeting Eya2.

Author information

1
Department of Endocrinology, Chinese PLA General Hospital, Chinese PLA Medical School, Beijing, People's Republic of China; Department of Medical Molecular Biology, Beijing Institute of Biotechnology, Beijing, People's Republic of China.
2
Department of Medical Molecular Biology, Beijing Institute of Biotechnology, Beijing, People's Republic of China.
3
Department of Nuclear Medicine, Peking University First Hospital, Beijing, People's Republic of China.
4
Department of General Surgery, 307 Hospital of PLA, Beijing, People's Republic of China.
5
Department of Endocrinology, Chinese PLA General Hospital, Chinese PLA Medical School, Beijing, People's Republic of China.
6
Beijing Institute of Radiation Medicine, Beijing, People's Republic of China.
7
Department of General Surgery, 307 Hospital of PLA, Beijing, People's Republic of China. Electronic address: yuchengze@sina.com.
8
Department of Medical Molecular Biology, Beijing Institute of Biotechnology, Beijing, People's Republic of China. Electronic address: yeqn66@yahoo.com.
9
Department of Endocrinology, Chinese PLA General Hospital, Chinese PLA Medical School, Beijing, People's Republic of China. Electronic address: metabolism301@126.com.

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.

KEYWORDS:

Breast cancer; Cell migration; Cell proliferation; Eya2; miR-30a

PMID:
24508260
DOI:
10.1016/j.bbrc.2014.01.174
[Indexed for MEDLINE]

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