MiR-200c is a cMyc-activated miRNA that promotes nasopharyngeal carcinoma by downregulating PTEN
Metrics: PDF 1633 views | HTML 2326 views | ?
Pan Chen1,2,*, Xiaofang Guo2,3,*, Liming Zhang2,4, Wenling Zhang2, Qingyu Zhou3, Zhi Tian3, Ying Zheng2, Qianjin Liao1,2, Heran Wang1,2, Guiyuan Li1,2, Jin Huang5, Xiayu Li6
1Hunan Cancer Hospital and The Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University, Changsha, Hunan 410013, China
2Key Laboratory of Carcinogenesis of Ministry of Health, Cancer Research Institute, Central South University, Xiangya Road, Changsha, Hunan 410078, China
3Department of Pharmaceutical Sciences, College of Pharmacy, University of South Florida, Tampa, FL33612, USA
4The Department of Laboratory Medicine, Huaihua Medical College, Huaihua, Hunan 418000, China
5Department of Oncology, Xiangya Hospital, Central South University, Changsha, Hunan 410078, China
6Hunan 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
Xiayu Li, email: [email protected]
Jin Huang, email: [email protected]
Keywords: miRNA-200c, c-Myc, PTEN, nasopharyngeal carcinoma
Received: May 12, 2016 Accepted: November 23, 2016 Published: December 23, 2016
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.
All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 4.0 License.