Open Access

miR‑210‑3p regulates the proliferation and apoptosis of non‑small cell lung cancer cells by targeting SIN3A

  • Authors:
    • Jie Ren
    • Xiaodan Li
    • Hao Dong
    • Longlong Suo
    • Jun Zhang
    • Lina Zhang
    • Jing Zhang
  • View Affiliations

  • Published online on: August 8, 2019     https://doi.org/10.3892/etm.2019.7867
  • Pages: 2565-2573
  • Copyright: © Ren et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Previous studies have indicated that microRNA (miR)‑210‑3p is upregulated in NSCLC, however, the specific mechanism underlying the role of miR‑210‑3p in NSCLC pathogenesis requires further investigation. The aim of the present study was to explore the roles of miR‑210‑3p in NSCLC and the associated mechanisms. A total of 30 NSCLC tissues and paired adjacent normal tissues were collected for study. Reverse transcription‑quantitative polymerase chain reaction was performed to compare the expression of miR‑210‑3p in the 30 paired cancerous and adjacent normal tissues. Additionally, the expression of miR‑210‑3p in different NSCLC lines and normal human lung epithelial cell line BEAS‑2B were also compared. Furthermore, A549 and H1299 NSCLC cells were cultured and transfected with miR‑210‑3p inhibitors, and MTT and propidium iodide/annexin V assays were performed to investigate the effects of miR‑210‑3p inhibition on the proliferation and apoptosis of the cells. RT‑qPCR and western blot analyses were also performed to determine the effects of miR‑210‑3p on the expression levels of SIN3A, B‑cell lymphoma 2 (Bcl‑2) and Caspase‑3. Finally, a reverse experiment was conducted by transfecting A549 cells with miR‑210‑3p inhibitor and SIN3A small interfering (si)RNA, and a dual‑luciferase reporter assay was performed to confirm that SIN3A is a direct target of miR‑210‑3p. It was observed that miR‑210‑3p was significantly upregulated in NSCLC tissues compared with the levels in the adjacent normal tissues, and that the expression of miR‑210‑3p in patients with NSCLC was negatively correlated with the expression of SIN3A in NSCLC tissue. miR‑210‑3p was also significantly upregulated in different NSCLC cell lines compared with the levels in BEAS‑2B cells. The transient downregulation of miR‑210‑3p in A549 cells led to a significant suppression of cell proliferation and markedly increased cell apoptosis, as well as increased the expression of SIN3A and Caspase‑3 and decreased the expression of Bcl‑2. On the other hand, co‑transfection of miR‑210‑3p inhibitor and SIN3A siRNA partially blocked miR‑210‑3p inhibitor‑induced pro‑apoptotic effects. The results of the dual‑luciferase reporter assay demonstrated that SIN3A is a direct target of miR‑210‑3p. Collectively, these findings indicate that can regulate the proliferation and apoptosis of NSCLC cells by targeting SIN3A. These results suggest that miR‑210‑3p has the potential to become a novel therapeutic target for the treatment of NSCLC.
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October-2019
Volume 18 Issue 4

Print ISSN: 1792-0981
Online ISSN:1792-1015

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Spandidos Publications style
Ren J, Li X, Dong H, Suo L, Zhang J, Zhang L and Zhang J: miR‑210‑3p regulates the proliferation and apoptosis of non‑small cell lung cancer cells by targeting SIN3A. Exp Ther Med 18: 2565-2573, 2019
APA
Ren, J., Li, X., Dong, H., Suo, L., Zhang, J., Zhang, L., & Zhang, J. (2019). miR‑210‑3p regulates the proliferation and apoptosis of non‑small cell lung cancer cells by targeting SIN3A. Experimental and Therapeutic Medicine, 18, 2565-2573. https://doi.org/10.3892/etm.2019.7867
MLA
Ren, J., Li, X., Dong, H., Suo, L., Zhang, J., Zhang, L., Zhang, J."miR‑210‑3p regulates the proliferation and apoptosis of non‑small cell lung cancer cells by targeting SIN3A". Experimental and Therapeutic Medicine 18.4 (2019): 2565-2573.
Chicago
Ren, J., Li, X., Dong, H., Suo, L., Zhang, J., Zhang, L., Zhang, J."miR‑210‑3p regulates the proliferation and apoptosis of non‑small cell lung cancer cells by targeting SIN3A". Experimental and Therapeutic Medicine 18, no. 4 (2019): 2565-2573. https://doi.org/10.3892/etm.2019.7867