Open Accessmir-101-3p is a key regulator of tumor metabolism in triple negative breast cancer targeting AMPK
Author(s) -
Peng Liu,
Feng Ye,
Xinhua Xie,
Xing Li,
Hailin Tang,
Shuaijie Li,
Xin Huang,
Cailu Song,
Wang Wei-dong,
Xiaoming Xie
Publication year - 2016
Publication title -
oncotarget
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.373
H-Index - 127
ISSN - 1949-2553
DOI - 10.18632/oncotarget.9072
Subject(s) - ampk , triple negative breast cancer , breast cancer , cancer research , gene knockdown , ectopic expression , medicine , cancer , cell growth , oncology , cell culture , biology , protein kinase a , microbiology and biotechnology , kinase , genetics
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.