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Article Open Access

Downregulation of GLUT3 impairs STYK1/NOK‑mediated metabolic reprogramming and proliferation in NIH‑3T3 cells

  • Authors:
    • Weiye Shi
    • Yu Fu
    • Yingze Wang
  • View Affiliations / Copyright

    Affiliations: Cell Engineering Laboratory, College of Biological Science and Engineering, Hebei University of Science and Technology, Shijiazhuang, Hebei 050018, P.R. China
    Copyright: © Shi et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Article Number: 527
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    Published online on: May 14, 2021
       https://doi.org/10.3892/ol.2021.12788
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Abstract

Serine threonine tyrosine kinase 1 (STYK1)/novel oncogene with kinase domain (NOK) has been demonstrated to promote cell carcinogenesis and tumorigenesis, as well as to strengthen cellular aerobic glycolysis, which is considered to be a defining hallmark of cancer. As the carriers of glucose into cells, glucose transporters (GLUTs) are important participants in cellular glucose metabolism and even tumorigenesis. However, to the best of our knowledge, the role of GLUTs in biological events caused by STYK1/NOK has not yet been reported. The present study assessed GLUT3 as a key transporter, and glucose consumption and lactate production assays revealed that downregulation of GLUT3 impaired STYK1/NOK‑induced augmented glucose uptake and lactate production, and RT‑qPCR and western blotting confirmed that GLUT3 knockdown attenuated the STYK1/NOK-induced increase in the expression levels of key enzymes implicated in glycolysis. Furthermore, MTT and Transwell assays demonstrated that STYK1/NOK‑triggered cell proliferation and migration were also markedly decreased following knockdown of GLUT3. To the best of our knowledge, the present study is the first to demonstrate that GLUT3 serves a prominent role in STYK1/NOK‑driven aerobic glycolysis and cell proliferation characteristics. These findings may provide a clue for the investigation of the oncogenic activity of STYK1/NOK and for the identification of potential tumor therapy targets associated with GLUT3.
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Copy and paste a formatted citation
Spandidos Publications style
Shi W, Fu Y and Wang Y: Downregulation of GLUT3 impairs STYK1/NOK‑mediated metabolic reprogramming and proliferation in NIH‑3T3 cells. Oncol Lett 22: 527, 2021.
APA
Shi, W., Fu, Y., & Wang, Y. (2021). Downregulation of GLUT3 impairs STYK1/NOK‑mediated metabolic reprogramming and proliferation in NIH‑3T3 cells. Oncology Letters, 22, 527. https://doi.org/10.3892/ol.2021.12788
MLA
Shi, W., Fu, Y., Wang, Y."Downregulation of GLUT3 impairs STYK1/NOK‑mediated metabolic reprogramming and proliferation in NIH‑3T3 cells". Oncology Letters 22.1 (2021): 527.
Chicago
Shi, W., Fu, Y., Wang, Y."Downregulation of GLUT3 impairs STYK1/NOK‑mediated metabolic reprogramming and proliferation in NIH‑3T3 cells". Oncology Letters 22, no. 1 (2021): 527. https://doi.org/10.3892/ol.2021.12788
Copy and paste a formatted citation
x
Spandidos Publications style
Shi W, Fu Y and Wang Y: Downregulation of GLUT3 impairs STYK1/NOK‑mediated metabolic reprogramming and proliferation in NIH‑3T3 cells. Oncol Lett 22: 527, 2021.
APA
Shi, W., Fu, Y., & Wang, Y. (2021). Downregulation of GLUT3 impairs STYK1/NOK‑mediated metabolic reprogramming and proliferation in NIH‑3T3 cells. Oncology Letters, 22, 527. https://doi.org/10.3892/ol.2021.12788
MLA
Shi, W., Fu, Y., Wang, Y."Downregulation of GLUT3 impairs STYK1/NOK‑mediated metabolic reprogramming and proliferation in NIH‑3T3 cells". Oncology Letters 22.1 (2021): 527.
Chicago
Shi, W., Fu, Y., Wang, Y."Downregulation of GLUT3 impairs STYK1/NOK‑mediated metabolic reprogramming and proliferation in NIH‑3T3 cells". Oncology Letters 22, no. 1 (2021): 527. https://doi.org/10.3892/ol.2021.12788
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