MiR‐181a mediates metabolic shift in colon cancer cells via the PTEN/AKT pathway. Issue 9 (28th March 2014)

• Record Type: Journal Article
• Authors: Wei, Zhonghua; Cui, Long; Mei, Zubing; Liu, Min; Zhang, Daoxiang
• Is Part Of: FEBS letters. Volume 588:Issue 9(2014)
• Page Start: 1773
• Page End: 1779
• Publication Date: 2014-03-28
• Subjects: miR-181a -- PTEN -- Glycolysis; Biochemistry -- Periodicals; Biophysics -- Periodicals; Molecular biology -- Periodicals; Biochimie -- Périodiques; Biochemistry; Biophysics; Molecular biology; Periodicals; 572.05
• DOI: 10.1016/j.febslet.2014.03.037
• Languages: English
• ISSNs: 0014-5793

Abstract

Abstract : 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. Abstract : miR‐181a is significantly overexpressed in colon cancer patient samples. Overexpression of miR‐181a in colon cancer cells can promote cell proliferation through the enhanced glycolysis. miR‐181a can suppress the expression of PTEN, thus leading to the increased activation of AKT to stimulate glycolysis.