Long non-coding RNA UCA1 promotes glycolysis by upregulating hexokinase 2 through the mTOR-STAT3/microRNA143 pathway.
Bottom Line: Emerging evidence has shown that long non-coding RNAs (lncRNAs) act as key regulators of multiple cancers.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.
Affiliation: Center for Translational Medicine, The First Affiliated Hospital, School of Medicine, Xi'an Jiaotong University, Xi'an, China.Show MeSH
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Mentions: Given that UCA1 promotes tumor initiation and malignant progression,(11) and that the reprogramming of energy metabolism is critical to the survival and proliferation of cancer cells,(15) we asked whether UCA1 potentiates cancer cell energy metabolism. To this end, we first examined the effect of UCA1 on glucose metabolism in bladder cancer cells. The results showed that overexpression of UCA1 dramatically increased the rates of glucose consumption and lactate production in UM-UC-2 cells (Fig. 1a–c). We also knocked down UCA1 in 5637 cells, which have high endogenous UCA1 expression, and found that the rates of glucose consumption and lactate production were significantly decreased in these cells (Fig. 1d–f). Collectively, these results indicate that UCA1 enhances glycolysis in bladder cancer cells.
Affiliation: Center for Translational Medicine, The First Affiliated Hospital, School of Medicine, Xi'an Jiaotong University, Xi'an, China.