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Cancer cells preferentially metabolize glucose through aerobic glycolysis, a phenomenon known as the Warburg effect. Emerging evidence has shown that long non‐coding  RNA s (lnc RNA s) act as key regulators of multiple cancers. However, it remains largely unexplored whether and how lnc RNA  regulates glucose metabolism in cancer cells. In this study, we show that lnc RNA UCA 1 promotes glycolysis in bladder cancer cells, and that  UCA 1‐induced hexokinase 2 ( HK 2) functions as an important mediator in this process. We further show that  UCA 1 activates  mTOR  to regulate  HK 2 through both activation of  STAT 3 and repression of micro RNA 143. 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.

Long non‐coding RNA UCA1 promotes glycolysis by upregulating hexokinase 2 through the mTOR –STAT3/microRNA143 pathway