Open AccessLong non‐coding RNA UCA1 promotes glycolysis by upregulating hexokinase 2 through the mTOR –STAT3/microRNA143 pathway
Author(s) -
Li Zhengkun,
Li Xu,
Wu Shouzhen,
Xue Mei,
Chen Wei
Publication year - 2014
Publication title -
cancer science
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.035
H-Index - 141
eISSN - 1349-7006
pISSN - 1347-9032
DOI - 10.1111/cas.12461
Subject(s) - pi3k/akt/mtor pathway , hexokinase , anaerobic glycolysis , rna , glycolysis , cancer cell , warburg effect , microbiology and biotechnology , biology , microrna , mediator , long non coding rna , chemistry , metabolism , cancer research , cancer , biochemistry , signal transduction , gene , genetics
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.