miR-181a mediates metabolic shift in colon cancer cells via the PTEN/AKT pathway.

FEBS Lett

Department of Pathology of Shanghai Jiao Tong University Affiliated Sixth People's Hospital, China; Department of Colorectal Surgery, Xinhua Hospital, Shanghai Jiao Tong University School of Medicine, China; Department of Biochemistry & Molecular Cell Biology, Shanghai Jiao Tong University School of Medicine, 280 South Chongqing Road, Shanghai 200025, China. Electronic address:

Published: May 2014

Cancer cell metabolism is often characterized by a shift from an oxidative to a glycolytic bioenergetics pathway, a phenomenon known as the warburg effect. Whether the deregulation of miRNAs contributes to the warburg effect remains largely unknown. Here we show that miR-181a expression is increased and thus induces a metabolic shift in colon cancer cells. miR-181a performs this function by inhibiting the expression of PTEN, leading to an increase of phosphorylated AKT which triggers metabolic shift. The increase of lactate production induced by miR-181a results in the rapid growth of cancer cells. These results identify miR-181a as a molecular switch involved in the orchestration of the warburg effect in colon cancer cells via the PTEN/AKT pathway.

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http://dx.doi.org/10.1016/j.febslet.2014.03.037DOI Listing

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