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Article

miR‑143 inhibits cell proliferation by targeting autophagy‑related 2B in non‑small cell lung cancer H1299 cells

  • Authors:
    • Jiali Wei
    • Zhongliang Ma
    • Yanli Li
    • Botao Zhao
    • Detao Wang
    • Yan Jin
    • Youxin Jin
  • View Affiliations / Copyright

    Affiliations: School of Life Sciences, Shanghai University, Shanghai 200444, P.R. China, Institute of Biomedicine and Biotechnology, Shenzhen Institutes of Advanced Technology, Chinese Academy of Sciences, Shenzhen, Guangdong 518055, P.R. China
  • Pages: 571-576
    |
    Published online on: October 16, 2014
       https://doi.org/10.3892/mmr.2014.2675
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Abstract

microRNAs (miRNAs) are small, non‑coding RNAs involved in multiple biological pathways by regulating post‑transcriptional gene expression. Previously, autophagy has been reported to suppress the progression of non‑small cell lung cancer (NSCLC). However, how miRNAs regulate autophagy in NSCLC remains to be elucidated. In the present study, the autophagy gene, autophagy‑related 2B (ATG2B), was identified as a novel target of miR‑143. The overexpression of miR‑143 was able to downregulate the expression of atg2b at the transcriptional and translational levels by direct binding to its 3' untranslated region. Cell proliferation was significantly inhibited by the ectopic expression of miR‑143 in H1299 cells. Knockdown of ATG2B resulted in a similar phenotype, with the overexpression of miR‑143 in NSCLC cells. Furthermore, knockdown of ATG2B and hexokinase 2, a key enzyme in glycolysis and another target of miR‑143, co‑ordinated to inhibit the proliferation of H1299 cells. The results of the present study demonstrated that miR‑143 was a novel and important regulator of autophagy by targeting ATG2B and repression of gene expression in autophagy and high glycolysis had a coordinate effect in H1299 cells. These results suggested that ATG2B may be a new potential therapeutic target for NSCLC. Furthermore, it was implied that interrupting autophagy and glycolysis improves NSCLC therapy.
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Copy and paste a formatted citation
Spandidos Publications style
Wei J, Ma Z, Li Y, Zhao B, Wang D, Jin Y and Jin Y: miR‑143 inhibits cell proliferation by targeting autophagy‑related 2B in non‑small cell lung cancer H1299 cells. Mol Med Rep 11: 571-576, 2015.
APA
Wei, J., Ma, Z., Li, Y., Zhao, B., Wang, D., Jin, Y., & Jin, Y. (2015). miR‑143 inhibits cell proliferation by targeting autophagy‑related 2B in non‑small cell lung cancer H1299 cells. Molecular Medicine Reports, 11, 571-576. https://doi.org/10.3892/mmr.2014.2675
MLA
Wei, J., Ma, Z., Li, Y., Zhao, B., Wang, D., Jin, Y., Jin, Y."miR‑143 inhibits cell proliferation by targeting autophagy‑related 2B in non‑small cell lung cancer H1299 cells". Molecular Medicine Reports 11.1 (2015): 571-576.
Chicago
Wei, J., Ma, Z., Li, Y., Zhao, B., Wang, D., Jin, Y., Jin, Y."miR‑143 inhibits cell proliferation by targeting autophagy‑related 2B in non‑small cell lung cancer H1299 cells". Molecular Medicine Reports 11, no. 1 (2015): 571-576. https://doi.org/10.3892/mmr.2014.2675
Copy and paste a formatted citation
x
Spandidos Publications style
Wei J, Ma Z, Li Y, Zhao B, Wang D, Jin Y and Jin Y: miR‑143 inhibits cell proliferation by targeting autophagy‑related 2B in non‑small cell lung cancer H1299 cells. Mol Med Rep 11: 571-576, 2015.
APA
Wei, J., Ma, Z., Li, Y., Zhao, B., Wang, D., Jin, Y., & Jin, Y. (2015). miR‑143 inhibits cell proliferation by targeting autophagy‑related 2B in non‑small cell lung cancer H1299 cells. Molecular Medicine Reports, 11, 571-576. https://doi.org/10.3892/mmr.2014.2675
MLA
Wei, J., Ma, Z., Li, Y., Zhao, B., Wang, D., Jin, Y., Jin, Y."miR‑143 inhibits cell proliferation by targeting autophagy‑related 2B in non‑small cell lung cancer H1299 cells". Molecular Medicine Reports 11.1 (2015): 571-576.
Chicago
Wei, J., Ma, Z., Li, Y., Zhao, B., Wang, D., Jin, Y., Jin, Y."miR‑143 inhibits cell proliferation by targeting autophagy‑related 2B in non‑small cell lung cancer H1299 cells". Molecular Medicine Reports 11, no. 1 (2015): 571-576. https://doi.org/10.3892/mmr.2014.2675
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