miR-124 downregulation leads to breast cancer progression via LncRNA-MALAT1 regulation and CDK4/E2F1 signal activation
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Tongbao Feng1,2,3, Fang Shao1, Qiyong Wu3, Xiaohang Zhang1, Dongqin Xu1, Keqing Qian1,2, Yewen Xie1,2, Shizhong Wang1, Ning Xu4, Yong Wang3, Chunjian Qi1,2
1Medical Research Center, The Affiliated Hospital of Nanjing Medical University, Changzhou No.2 People’s Hospital, Changzhou, 213003, China
2Department of Oncology, The Affiliated Hospital of Nanjing Medical University, Changzhou No.2 People’s Hospital, Changzhou, 213003, China
3Department of General Surgery, the Affiliated Hospital of Nanjing Medical University, Changzhou No.2 People’s Hospital, Changzhou, 213003, China
4Section of Clinical Chemistry and Pharmacology, Department of Laboratory Medicine, Lund University, S-221 85 Lund, Sweden
Chunjian Qi, e-mail: email@example.com
Keywords: miR-124, MALAT1, cyclin-dependent kinase 4, cell cycle, breast cancer
Received: November 01, 2015 Accepted: February 05, 2016 Published: February 22, 2016
The long non-coding RNA (lncRNA) metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) has been recently shown to be dysregulated in several cancers. However, the mechanisms underlying the role of MALAT1 in breast cancer remain unclear. Herein, we showed that MALAT1 was aberrantly increased in breast cancer tissues and cells. MALAT1-siRNA inhibited breast cancer cell proliferation and cell cycle progression in vitro and in vivo. Furthermore, MALAT1 acted as an endogenous potent regulator by directly binding to miR-124 and down-regulating miR-124 expression. In addition, MALAT1 reversed the inhibitory effect of miR-124 on breast cancer proliferation and was involved in the cyclin-dependent kinase 4 (CDK4) expression. Taken together, our data highlight the pivotal role of MALAT1 in breast cancer tumorigenesis. Moreover, the present study elucidated the MALAT1-miR-124-CDK4/E2F1 signaling pathway in breast cancer, which might provide a new approach for tackling breast cancer.
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