Long non‐coding RNA UCA1 promotes glycolysis by upregulating hexokinase 2 through the mTOR–STAT3/microRNA143 pathway. Issue 8 (August 2014)

• Record Type: Journal Article
• Authors: Li, Zhengkun; Li, Xu; Wu, Shouzhen; Xue, Mei; Chen, Wei
• Is Part Of: Cancer science. Volume 105:Issue 8(2014:Aug.)
• Page Start: 951
• Page End: 955
• Publication Date: 2014-08
• Subjects: Cancer -- Periodicals; Neoplasms -- Periodicals; Research -- Periodicals; Electronic journals; 616.994005
• DOI: 10.1111/cas.12461
• Languages: English
• ISSNs: 1347-9032

Abstract

<abstract abstract-type="main" id="cas12461-abs-0001"> <title> <x xml:space="preserve">Abstract</x> </title> <p>Cancer cells preferentially metabolize glucose through aerobic glycolysis, a phenomenon known as the Warburg effect. Emerging evidence has shown that long non‐coding RNAs (lncRNAs) act as key regulators of multiple cancers. However, it remains largely unexplored whether and how lncRNA regulates glucose metabolism in cancer cells. In this study, we show that lncRNA UCA1 promotes glycolysis in bladder cancer cells, and that UCA1‐induced hexokinase 2 (HK2) functions as an important mediator in this process. We further show that UCA1 activates mTOR to regulate HK2 through both activation of STAT3 and repression of microRNA143. Taken together, these findings provide the first evidence that UCA1 plays a positive role in cancer cell glucose metabolism through the cascade of mTOR–STAT3/microRNA143–HK2, and reveal a novel link between lncRNA and the altered glucose metabolism in cancer cells.</p> </abstract>