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Myocardin inhibits estrogen receptor alpha‐mediated proliferation of human breast cancer MCF‐7 cells via regulating MicroRNA expression
Author(s) -
Xiang Yuan,
Lu DaLin,
Li JiaPeng,
Yu ChengXi,
Zheng DeLiang,
Huang Xuan,
Wang ZhenYu,
Hu Peng,
Liao XingHua,
Zhang TongCun
Publication year - 2016
Publication title -
iubmb life
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.132
H-Index - 113
eISSN - 1521-6551
pISSN - 1521-6543
DOI - 10.1002/iub.1507
Subject(s) - myocardin , cancer research , mcf 7 , microrna , cell growth , estrogen receptor , breast cancer , biology , chemistry , cancer , transcription factor , medicine , human breast , serum response factor , biochemistry , gene
Myocardin is frequently repressed during human malignant transformation, and restoration of myocardin expression in sarcoma cells contributes to the inhibition of malignant growth. However, its role in breast carcinoma has barely been addressed. Here, we reported that myocardin could inhibit the proliferation of MCF‐7 cells. Notably, we show that myocardin inhibited ERα‐mediated proliferation of breast cancer MCF‐7 via impairing ER‐dependent transcriptional activation, mainly through the inhibition of the activity of ERα. Importantly, the molecular mechanism for the inhibition of the ERα‐mediated proliferation is that myocardin inhibited the transcription and expression of ERα‐induced PCNA, Ki‐67, and E2F1 to impair ERα‐mediated proliferation of breast cancer MCF‐7. Interestingly, myocardin significantly enhanced the transcription and expression of miR‐885 depending on the CArG box in miR‐885 promoter, and miR‐885 targeted the 3′ untranslated regions (UTR) of E2F1 to silence the expression of E2F1. Thus, our data provided important and novel insights into how myocardin may deeply influence ERα‐mediated breast cancer proliferation. In conclusion, myocardin could be seen as a breast cancer tumor suppressor so that it will provide new ideas for the treatment of breast cancer. © 2016 IUBMB Life, 68(6):477–487, 2016