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miR‑218 inhibits glucose metabolism in non‑small cell lung cancer via the NF‑κB signaling pathway

  • Authors:
    • Wenxian Tian
    • Xiangfei Yuan
    • Yongna Song
    • Jianxia Zhai
    • Haixia Wei
    • Linna Wang
    • Dan Li
    • Qiusheng Chen
  • View Affiliations / Copyright

    Affiliations: Department of Pulmonary and Critical Care Medicine, Zhengzhou Central Hospital Affiliated to Zhengzhou University, Zhengzhou, Henan 450000, P.R. China, Tianjin Key Laboratory of Acute Abdomen Disease Associated Organ Injury and Institute of Traditional Chinese and Western Medicine, Institute of Acute Abdominal Diseases, Tianjin Nankai Hospital, Tianjin 300100, P.R. China
  • Article Number: 106
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    Published online on: November 27, 2020
       https://doi.org/10.3892/etm.2020.9538
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Abstract

High glucose metabolism is recognized as one of the hallmarks of cancer and increased expression levels of several key factors involved in glucose metabolism have been reported in non‑small cell lung cancer (NSCLC). Previous studies showed that microRNA (miR)‑218 is reduced in NSCLC, but its function in glucose metabolism in NSCLC is not fully understood. The present study aimed to investigate the effect of miR‑218 on glucose metabolism in NSCLC cell lines and the underlying molecular mechanism. The present results suggested that miR‑218 reduced glucose consumption, the mechanism of glycolysis and activity in the pentose phosphate pathway. In addition, glucose transporter 1 (GLUT1) was identified to be a direct target of miR‑218, while overexpression of GLUT1 did not abolish the effect of miR‑218 on glucose metabolism. The present results indicated that phosphorylation of NF‑κB p65 was significantly decreased by miR‑218 in NSCLC cells and that activation of NF‑κB led to the inhibition of miR‑218 regulation of glucose metabolism. In conclusion, the present results suggested that miR‑218 downregulated glucose metabolism in NSCLC not only by directly targeting GLUT1, but also via the NF‑κB signaling pathway.
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Copy and paste a formatted citation
Spandidos Publications style
Tian W, Yuan X, Song Y, Zhai J, Wei H, Wang L, Li D and Chen Q: miR‑218 inhibits glucose metabolism in non‑small cell lung cancer via the NF‑κB signaling pathway. Exp Ther Med 21: 106, 2021.
APA
Tian, W., Yuan, X., Song, Y., Zhai, J., Wei, H., Wang, L. ... Chen, Q. (2021). miR‑218 inhibits glucose metabolism in non‑small cell lung cancer via the NF‑κB signaling pathway. Experimental and Therapeutic Medicine, 21, 106. https://doi.org/10.3892/etm.2020.9538
MLA
Tian, W., Yuan, X., Song, Y., Zhai, J., Wei, H., Wang, L., Li, D., Chen, Q."miR‑218 inhibits glucose metabolism in non‑small cell lung cancer via the NF‑κB signaling pathway". Experimental and Therapeutic Medicine 21.2 (2021): 106.
Chicago
Tian, W., Yuan, X., Song, Y., Zhai, J., Wei, H., Wang, L., Li, D., Chen, Q."miR‑218 inhibits glucose metabolism in non‑small cell lung cancer via the NF‑κB signaling pathway". Experimental and Therapeutic Medicine 21, no. 2 (2021): 106. https://doi.org/10.3892/etm.2020.9538
Copy and paste a formatted citation
x
Spandidos Publications style
Tian W, Yuan X, Song Y, Zhai J, Wei H, Wang L, Li D and Chen Q: miR‑218 inhibits glucose metabolism in non‑small cell lung cancer via the NF‑κB signaling pathway. Exp Ther Med 21: 106, 2021.
APA
Tian, W., Yuan, X., Song, Y., Zhai, J., Wei, H., Wang, L. ... Chen, Q. (2021). miR‑218 inhibits glucose metabolism in non‑small cell lung cancer via the NF‑κB signaling pathway. Experimental and Therapeutic Medicine, 21, 106. https://doi.org/10.3892/etm.2020.9538
MLA
Tian, W., Yuan, X., Song, Y., Zhai, J., Wei, H., Wang, L., Li, D., Chen, Q."miR‑218 inhibits glucose metabolism in non‑small cell lung cancer via the NF‑κB signaling pathway". Experimental and Therapeutic Medicine 21.2 (2021): 106.
Chicago
Tian, W., Yuan, X., Song, Y., Zhai, J., Wei, H., Wang, L., Li, D., Chen, Q."miR‑218 inhibits glucose metabolism in non‑small cell lung cancer via the NF‑κB signaling pathway". Experimental and Therapeutic Medicine 21, no. 2 (2021): 106. https://doi.org/10.3892/etm.2020.9538
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