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Article Open Access

Specific protein 1 depletion attenuates glucose uptake and proliferation of human glioma cells by regulating GLUT3 expression

  • Authors:
    • Chuanyi Zheng
    • Kun Yang
    • Maoying Zhang
    • Mingming Zou
    • Enqi Bai
    • Quanhong Ma
    • Ruxiang Xu
  • View Affiliations / Copyright

    Affiliations: Affiliated Bayi Brain Hospital, General Hospital of Beijing Military Region, Southern Medical University, Beijing 100072, P.R. China, Department of Neurosurgery, The Affiliated Hospital of Hainan Medical College, Haikou, Hainan 570102, P.R. China, Jiangsu Key Laboratory of Translational Research and Therapy for Neuro‑Psycho‑Diseases, Institute of Neuroscience, Soochow University, Suzhou, Jiangsu 215123, P.R. China
    Copyright: © Zheng et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Pages: 125-131
    |
    Published online on: May 17, 2016
       https://doi.org/10.3892/ol.2016.4599
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Abstract

It has been reported previously that the expression of glucose transporter member 3 (GLUT3) is increased in malignant glioma cells compared with normal glial cells. However, the regulating mechanism that causes this phenomenon remains unknown. The present study investigated the regulating role of transcription factor specific protein 1 (Sp1) in GLUT3 expression in a human glioma cell line. In the present study, Sp1 was identified to directly bind to the GLUT3 5'‑untranslated region in human glioma U251 cells. Small interfering RNA‑ and the Sp1-inhibitor mithramycin A-mediated Sp1 knockdown experiments revealed that Sp1 depletion decreased glucose uptake and inhibited cell growth and invasion of U251 cells by downregulating GLUT3 expression. Therefore Sp1 is an important positive regulator for the expression of GLUT3 in human glioma cells, and may explain the overexpression of GLUT3 in U251 cells. These results suggest that Sp1 may have a role in glioma treatment.
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Copy and paste a formatted citation
Spandidos Publications style
Zheng C, Yang K, Zhang M, Zou M, Bai E, Ma Q and Xu R: Specific protein 1 depletion attenuates glucose uptake and proliferation of human glioma cells by regulating GLUT3 expression. Oncol Lett 12: 125-131, 2016.
APA
Zheng, C., Yang, K., Zhang, M., Zou, M., Bai, E., Ma, Q., & Xu, R. (2016). Specific protein 1 depletion attenuates glucose uptake and proliferation of human glioma cells by regulating GLUT3 expression. Oncology Letters, 12, 125-131. https://doi.org/10.3892/ol.2016.4599
MLA
Zheng, C., Yang, K., Zhang, M., Zou, M., Bai, E., Ma, Q., Xu, R."Specific protein 1 depletion attenuates glucose uptake and proliferation of human glioma cells by regulating GLUT3 expression". Oncology Letters 12.1 (2016): 125-131.
Chicago
Zheng, C., Yang, K., Zhang, M., Zou, M., Bai, E., Ma, Q., Xu, R."Specific protein 1 depletion attenuates glucose uptake and proliferation of human glioma cells by regulating GLUT3 expression". Oncology Letters 12, no. 1 (2016): 125-131. https://doi.org/10.3892/ol.2016.4599
Copy and paste a formatted citation
x
Spandidos Publications style
Zheng C, Yang K, Zhang M, Zou M, Bai E, Ma Q and Xu R: Specific protein 1 depletion attenuates glucose uptake and proliferation of human glioma cells by regulating GLUT3 expression. Oncol Lett 12: 125-131, 2016.
APA
Zheng, C., Yang, K., Zhang, M., Zou, M., Bai, E., Ma, Q., & Xu, R. (2016). Specific protein 1 depletion attenuates glucose uptake and proliferation of human glioma cells by regulating GLUT3 expression. Oncology Letters, 12, 125-131. https://doi.org/10.3892/ol.2016.4599
MLA
Zheng, C., Yang, K., Zhang, M., Zou, M., Bai, E., Ma, Q., Xu, R."Specific protein 1 depletion attenuates glucose uptake and proliferation of human glioma cells by regulating GLUT3 expression". Oncology Letters 12.1 (2016): 125-131.
Chicago
Zheng, C., Yang, K., Zhang, M., Zou, M., Bai, E., Ma, Q., Xu, R."Specific protein 1 depletion attenuates glucose uptake and proliferation of human glioma cells by regulating GLUT3 expression". Oncology Letters 12, no. 1 (2016): 125-131. https://doi.org/10.3892/ol.2016.4599
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