MiR-200c is a cMyc-activated miRNA that promotes nasopharyngeal carcinoma by downregulating PTEN

2017 
// Pan Chen 1, 2, * , Xiaofang Guo 2, 3, * , Liming Zhang 2, 4 , Wenling Zhang 2 , Qingyu Zhou 3 , Zhi Tian 3 , Ying Zheng 2 , Qianjin Liao 1, 2 , Heran Wang 1, 2 , Guiyuan Li 1, 2 , Jin Huang 5 , Xiayu Li 6 1 Hunan Cancer Hospital and The Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University, Changsha, Hunan 410013, China 2 Key Laboratory of Carcinogenesis of Ministry of Health, Cancer Research Institute, Central South University, Xiangya Road, Changsha, Hunan 410078, China 3 Department of Pharmaceutical Sciences, College of Pharmacy, University of South Florida, Tampa, FL33612, USA 4 The Department of Laboratory Medicine, Huaihua Medical College, Huaihua, Hunan 418000, China 5 Department of Oncology, Xiangya Hospital, Central South University, Changsha, Hunan 410078, China 6 Hunan Key Laboratory of Nonresolving Inflammation and Cancer, Disease Genome Research Center, The Third Xiangya Hospital, Central South University, Changsha, Hunan 410013, China * These authors have contributed equally to this work Correspondence to: Xiayu Li, email: lixiayu@163.com Jin Huang, email: jinhuang@csu.edu.cn Keywords: miRNA-200c, c-Myc, PTEN, nasopharyngeal carcinoma Received: May 12, 2016     Accepted: November 23, 2016     Published: December 23, 2016 ABSTRACT The c-Myc transcription factor regulates a complex transcriptional program that leads to cellular transformation by targeting a large number of protein-encoding genes and non-coding RNAs. In this study, we show that a microRNA, miR-200c, is a novel c-Myc target that promotes cellular transformation and metastasis in nasopharyngeal carcinoma. MiR-200c achieves this oncogenic effect, at least in part, by targeting and inhibiting the tumor suppressor gene PTEN (phosphatase and tensin homolog), which is a key inhibitor of the AKT kinase signaling that promotes tumorigenesis in nasopharyngeal carcinoma. Our study thus identifies cMyc-miR-200c-PTEN-AKT as a functional module that promotes cellular transformation in nasopharyngeal carcinoma.
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