Demethylation of the MIR145 promoter suppresses migration and invasion in breast cancer
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Shui-Yi Liu1,2,*, Xiao-Yi Li1,*, Wei-Qun Chen1,2,3,*, Hui Hu1, Bo Luo6, Yu-Xiang Shi6, Tang-Wei Wu1, Yong Li1,7, Qing-Zhi Kong2,3,4,5, Hong-Da Lu2,3,4,5 and Zhong-Xin Lu1,2,3,4
1Department of Medical Laboratory, Central Hospital of Wuhan, Wuhan 430014, China
2Cancer Research Institute of Wuhan, Wuhan 430014, China
3Department of Central Laboratory, Central Hospital of Wuhan, Wuhan 430014, China
4Key Laboratory for Molecular Diagnosis of Hubei Province, Central Hospital of Wuhan, Wuhan 430014, China
5Department of Oncology, Central Hospital of Wuhan, Wuhan 430014, China
6Department of Pathology, Central Hospital of Wuhan, Wuhan 430014, China
7Department of Cancer Biology, Lerner Research Institute, Cleveland Clinic, Cleveland, OH 44195, USA
*These authors have contributed equally to this work
Zhong-Xin Lu, email: email@example.com
Hong-Da Lu, email: firstname.lastname@example.org
Keywords: miR-145, methylation, breast cancer, ANGPT2, migration and invasion
Received: November 04, 2016 Accepted: May 12, 2017 Published: June 27, 2017
miR-145 has been implicated in the progression of breast cancer. Here, we report that its expression is decreased in breast cancer specimens and cell lines and that this low level of expression is associated with DNA methylation of its gene, MIR145. Methylation of MIR145 has previously been correlated with cell migration and invasion, both in vivo and in vitro. We found that demethylation of MIR145 reactivates miR-145 and contributes to the anti-cancer properties of 5-aza-2′-deoxyazacytidine (5-AzaC). Therefore, miR-145 is a potentially valuable biomarker for breast cancer.
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