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

Li Z, Li X, Wu S, Xue M, Chen W - Cancer Sci. (2014)

Bottom Line: 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.We further show that UCA1 activates mTOR to regulate HK2 through both activation of STAT3 and repression of microRNA143.

View Article: PubMed Central - PubMed

Affiliation: Center for Translational Medicine, The First Affiliated Hospital, School of Medicine, Xi'an Jiaotong University, Xi'an, China.

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Long non-coding RNA UCA1 promotes glycolysis in bladder cancer cells. (a, d) Quantitative PCR analysis of UCA1 expression in stable cell lines. UMUC-2 cells were transfected with pcDNA3.1/UCA1 (pcDNA-U) and pcDNA3.1/Mock (pcDNA-M) plasmids (a); 5637 cells were transfected with pRNAT-U6.1/Neo-shUCA (pRNAT-U) and pRNAT-U6.1/Neo-Nc (pRNAT-N) plasmids (d). (b, c, e, f) Glucose consumption and lactate production were analyzed in stable cell lines with overexpression of UCA1 (b, c) and knockdown of UCA1 (e, f). The average values ± SD of three separate experiments were plotted. *P < 0.05.
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fig01: Long non-coding RNA UCA1 promotes glycolysis in bladder cancer cells. (a, d) Quantitative PCR analysis of UCA1 expression in stable cell lines. UMUC-2 cells were transfected with pcDNA3.1/UCA1 (pcDNA-U) and pcDNA3.1/Mock (pcDNA-M) plasmids (a); 5637 cells were transfected with pRNAT-U6.1/Neo-shUCA (pRNAT-U) and pRNAT-U6.1/Neo-Nc (pRNAT-N) plasmids (d). (b, c, e, f) Glucose consumption and lactate production were analyzed in stable cell lines with overexpression of UCA1 (b, c) and knockdown of UCA1 (e, f). The average values ± SD of three separate experiments were plotted. *P < 0.05.

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.


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

Li Z, Li X, Wu S, Xue M, Chen W - Cancer Sci. (2014)

Long non-coding RNA UCA1 promotes glycolysis in bladder cancer cells. (a, d) Quantitative PCR analysis of UCA1 expression in stable cell lines. UMUC-2 cells were transfected with pcDNA3.1/UCA1 (pcDNA-U) and pcDNA3.1/Mock (pcDNA-M) plasmids (a); 5637 cells were transfected with pRNAT-U6.1/Neo-shUCA (pRNAT-U) and pRNAT-U6.1/Neo-Nc (pRNAT-N) plasmids (d). (b, c, e, f) Glucose consumption and lactate production were analyzed in stable cell lines with overexpression of UCA1 (b, c) and knockdown of UCA1 (e, f). The average values ± SD of three separate experiments were plotted. *P < 0.05.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4317864&req=5

fig01: Long non-coding RNA UCA1 promotes glycolysis in bladder cancer cells. (a, d) Quantitative PCR analysis of UCA1 expression in stable cell lines. UMUC-2 cells were transfected with pcDNA3.1/UCA1 (pcDNA-U) and pcDNA3.1/Mock (pcDNA-M) plasmids (a); 5637 cells were transfected with pRNAT-U6.1/Neo-shUCA (pRNAT-U) and pRNAT-U6.1/Neo-Nc (pRNAT-N) plasmids (d). (b, c, e, f) Glucose consumption and lactate production were analyzed in stable cell lines with overexpression of UCA1 (b, c) and knockdown of UCA1 (e, f). The average values ± SD of three separate experiments were plotted. *P < 0.05.
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.

Bottom Line: 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.We further show that UCA1 activates mTOR to regulate HK2 through both activation of STAT3 and repression of microRNA143.

View Article: PubMed Central - PubMed

Affiliation: Center for Translational Medicine, The First Affiliated Hospital, School of Medicine, Xi'an Jiaotong University, Xi'an, China.

Show MeSH
Related in: MedlinePlus