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Article

Promotion of glycolysis by HOTAIR through GLUT1 upregulation via mTOR signaling

  • Authors:
    • Shibo Wei
    • Qing Fan
    • Liang Yang
    • Xiaodong Zhang
    • Yingbo Ma
    • Zhihong Zong
    • Xiangdong Hua
    • Dongming Su
    • Hongzhi Sun
    • Hangyu Li
    • Zhen Liu
  • View Affiliations / Copyright

    Affiliations: Department of General Surgery, The Shengjing Hospital Affiliated to China Medical University, Shenyang, Liaoning 110004, P.R. China, Department of General Surgery, The Fourth Affiliated Hospital of China Medical University, Shenyang, Liaoning 110032, P.R. China, Department of Biochemistry and Molecular Biology, College of Basic Medical Sciences, China Medical University, Shenyang, Liaoning 110001, P.R. China, Department of General Surgery, Liaoning Cancer Hospital and Institute, Shenyang, Liaoning 110042, P.R. China, Center of Metabolic Disease Research, Nanjing Medical University, Nanjing, Jiangsu 210029, P.R. China, Department of General Surgery, The First Hospital Affiliated to Jinzhou Medical College, Jinzhou, Liaoning 121001, P.R. China
  • Pages: 1902-1908
    |
    Published online on: July 20, 2017
       https://doi.org/10.3892/or.2017.5840
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Abstract

The long non-coding RNA HOX transcript antisense RNA (HOTAIR) plays a key role in the progression of various carcinomas. However, whether or not HOTAIR influences glucose metabolism and the specific underlying mechanism in hepatocellular carcinoma (HCC) cells remain unclear. In the present study, we found markedly increased HOTAIR expression in 84 HCC tissues and demonstrated that HOTAIR overexpression promoted cell proliferation using Cell Counting Kit-8. The effect on glucose metabolism regulated by HOTAIR in HCC cells was determined by detecting lactate and glucose levels: HOTAIR promoted glycolysis by upregulating glucose transporter isoform 1 (GLUT1) and activating mammalian target of rapamycin (mTOR) signaling, whereas knockdown of HOTAIR suppressed this effect. Our research reveals a novel relationship between HOTAIR and glucose metabolism in HCC cells, and it may be a therapeutic target for diagnosing and treating HCC.
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Copy and paste a formatted citation
Spandidos Publications style
Wei S, Fan Q, Yang L, Zhang X, Ma Y, Zong Z, Hua X, Su D, Sun H, Li H, Li H, et al: Promotion of glycolysis by HOTAIR through GLUT1 upregulation via mTOR signaling. Oncol Rep 38: 1902-1908, 2017.
APA
Wei, S., Fan, Q., Yang, L., Zhang, X., Ma, Y., Zong, Z. ... Liu, Z. (2017). Promotion of glycolysis by HOTAIR through GLUT1 upregulation via mTOR signaling. Oncology Reports, 38, 1902-1908. https://doi.org/10.3892/or.2017.5840
MLA
Wei, S., Fan, Q., Yang, L., Zhang, X., Ma, Y., Zong, Z., Hua, X., Su, D., Sun, H., Li, H., Liu, Z."Promotion of glycolysis by HOTAIR through GLUT1 upregulation via mTOR signaling". Oncology Reports 38.3 (2017): 1902-1908.
Chicago
Wei, S., Fan, Q., Yang, L., Zhang, X., Ma, Y., Zong, Z., Hua, X., Su, D., Sun, H., Li, H., Liu, Z."Promotion of glycolysis by HOTAIR through GLUT1 upregulation via mTOR signaling". Oncology Reports 38, no. 3 (2017): 1902-1908. https://doi.org/10.3892/or.2017.5840
Copy and paste a formatted citation
x
Spandidos Publications style
Wei S, Fan Q, Yang L, Zhang X, Ma Y, Zong Z, Hua X, Su D, Sun H, Li H, Li H, et al: Promotion of glycolysis by HOTAIR through GLUT1 upregulation via mTOR signaling. Oncol Rep 38: 1902-1908, 2017.
APA
Wei, S., Fan, Q., Yang, L., Zhang, X., Ma, Y., Zong, Z. ... Liu, Z. (2017). Promotion of glycolysis by HOTAIR through GLUT1 upregulation via mTOR signaling. Oncology Reports, 38, 1902-1908. https://doi.org/10.3892/or.2017.5840
MLA
Wei, S., Fan, Q., Yang, L., Zhang, X., Ma, Y., Zong, Z., Hua, X., Su, D., Sun, H., Li, H., Liu, Z."Promotion of glycolysis by HOTAIR through GLUT1 upregulation via mTOR signaling". Oncology Reports 38.3 (2017): 1902-1908.
Chicago
Wei, S., Fan, Q., Yang, L., Zhang, X., Ma, Y., Zong, Z., Hua, X., Su, D., Sun, H., Li, H., Liu, Z."Promotion of glycolysis by HOTAIR through GLUT1 upregulation via mTOR signaling". Oncology Reports 38, no. 3 (2017): 1902-1908. https://doi.org/10.3892/or.2017.5840
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