Open Access

Let‑7a inhibits proliferation and promotes apoptosis of human asthmatic airway smooth muscle cells

  • Authors:
    • Yan Chen
    • Lujun Qiao
    • Zewen Zhang
    • Guoxin Hu
    • Jian Zhang
    • Hongjia Li
  • View Affiliations

  • Published online on: March 7, 2019     https://doi.org/10.3892/etm.2019.7363
  • Pages: 3327-3334
  • Copyright: © Chen et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

The present study aimed to examine the changes of let‑7a expression in asthmatic airway smooth muscle cells (ASMCs) and to analyze its effect on the proliferation and apoptosis of ASMCs, as well as the potential mechanism of action. let‑7a expression levels in ASMCs from asthmatic and non‑asthmatic subjects were detected using reverse transcription‑quantitative polymerase chain reaction (RT‑qPCR) analysis. Furthermore, let‑7a mimics were transfected in vitro into ASMCs isolated from asthmatic patients, and the effect of let‑7a on ASMC proliferation was examined using a Cell Counting Kit‑8. In addition, the influence of let‑7a on ASMC apoptosis was detected using flow cytometry and a caspase‑3/7 activity assay. Target genes of let‑7a were predicted using bioinformatics software, and the direct regulatory effect of let‑7a on the potential target gene signal transducer and activator of transcription 3 (STAT3) was verified through a dual‑luciferase reporter gene assay combined with RT‑qPCR and western blot analysis. The results demonstrated that let‑7a expression was significantly lower in ASMCs of asthmatic subjects compared with that in ASMCs of normal subjects. Furthermore, upregulation of let‑7a expression in asthmatic ASMCs markedly inhibited cell proliferation and promoted cell apoptosis. The results of the dual‑luciferase reporter gene assay indicated that let‑7a selectively binds with the 3'‑untranslated region of the STAT3 mRNA. In addition, let‑7a mimics evidently reduced the mRNA and protein expression levels of STAT3 in asthmatic ASMCs. In conclusion, the present study demonstrates that let‑7a expression is downregulated in ASMCs from asthmatic patients. Furthermore, let‑7a suppresses the proliferation and promotes apoptosis of human asthmatic ASMCs, which may, at least partially, be associated with the downregulation of STAT3 expression.
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May-2019
Volume 17 Issue 5

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

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Spandidos Publications style
Chen Y, Qiao L, Zhang Z, Hu G, Zhang J and Li H: Let‑7a inhibits proliferation and promotes apoptosis of human asthmatic airway smooth muscle cells. Exp Ther Med 17: 3327-3334, 2019.
APA
Chen, Y., Qiao, L., Zhang, Z., Hu, G., Zhang, J., & Li, H. (2019). Let‑7a inhibits proliferation and promotes apoptosis of human asthmatic airway smooth muscle cells. Experimental and Therapeutic Medicine, 17, 3327-3334. https://doi.org/10.3892/etm.2019.7363
MLA
Chen, Y., Qiao, L., Zhang, Z., Hu, G., Zhang, J., Li, H."Let‑7a inhibits proliferation and promotes apoptosis of human asthmatic airway smooth muscle cells". Experimental and Therapeutic Medicine 17.5 (2019): 3327-3334.
Chicago
Chen, Y., Qiao, L., Zhang, Z., Hu, G., Zhang, J., Li, H."Let‑7a inhibits proliferation and promotes apoptosis of human asthmatic airway smooth muscle cells". Experimental and Therapeutic Medicine 17, no. 5 (2019): 3327-3334. https://doi.org/10.3892/etm.2019.7363