mir-101-3p is a key regulator of tumor metabolism in triple negative breast cancer targeting AMPK
Metrics: PDF 1698 views | HTML 1660 views | ?
Peng Liu1,2,*, Feng Ye1,2,*, Xinhua Xie1,2,*, Xing Li1,2, Hailin Tang1,2, Shuaijie Li1,2, Xiaojia Huang1,2, Cailu Song1,2, Weidong Wei1,2, Xiaoming Xie1,2
1Department of Breast Oncology, Sun Yat-Sen University Cancer Center, Guangzhou, Guangdong, People’s Republic of China
2State Key Laboratory of Oncology in South China, Sun Yat-Sen University Cancer Center, Collaborative Innovation Center for Cancer Medicine, Guangzhou, Guangdong, People’s Republic of China
*These authors have contributed equally to this work
Xiaoming Xie, e-mail: email@example.com
Weidong Wei, e-mail: firstname.lastname@example.org
Keywords: mir-101-3p, AMPK, triple negative breast cancer, tumor metabolism
Received: November 16, 2015 Accepted: March 28, 2016 Published: April 28, 2016
mir-101-3p has been reported to be a tumor suppressor and a promising therapeutic target in cancer. Recently, AMPK dysfunction has been highlighted in cancers, including breast cancer. The aim of this study is to investigate the biological roles of mir-101-3p and AMPK in breast cancer. Our research demonstrated that AMPK was up-regulated in breast cancer tissues and cell lines, especially in triple negative breast cancer (TNBC). High-expression of AMPK correlated with poor outcome in both total breast cancer and TNBC patients. Ectopic expression of AMPK improved glucose uptake, glycolysis, proliferation of TNBC cells in vitro and its tumorigenicity in vivo. AMPK was predicted to be a direct target of mir-101-3p. The luciferase reporter assay was performed to certificate this prediction. The expression of AMPK was suppressed by transfection of mir-101-3p in TNBC cells. Over-expression of mir-101-3p or knock-down of AMPK inhibited glucose metabolism and proliferation of TNBC cells in vitro. Our study provides evidence that mir-101-3p- AMPK axis could be a promising therapeutic target in TNBC targeting tumor metabolism.
All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 3.0 License.