MicroRNA‑320a inhibition decreases insulin‑induced KGN cell proliferation and apoptosis by targeting PCGF1

  • Authors:
    • Lei Yang
    • Yan Li
    • Xiaojing Wang
    • Yuling Liu
    • Lingzhu Yang
  • View Affiliations

  • Published online on: August 17, 2017     https://doi.org/10.3892/mmr.2017.7270
  • Pages: 5706-5712
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Abstract

MicroRNAs (miRNAs) are widely involved in regulation of cellular processes of polycystic ovary syndrome (PCOS). However, the function of miR‑320a in PCOS remains unclear. The present study aimed to explore the effect of miR‑320a on PCOS cell proliferation and apoptosis following treatment with insulin, and to clarify the underlying mechanism. PCOS tissues and corresponding normal tissues were collected from 16 female patients with PCOS. KGN cells were pre‑treated with insulin, and KGN cells were transfected with ASO‑miR‑320a, miR‑320a mimics and polycomb group ring finger 1 (PCGF1) overexpression plasmids. Expressions of miR‑320a and PCGF1 were detected using the reverse transcription‑quantitative polymerase chain reaction (RT‑qPCR). Dual‑Luciferase reporter assays were performed to investigate the target gene of miR‑320a. MTS, colony formation and flow cytometry assays were performed to determine cell viability, colony formation, and apoptosis, respectively. Furthermore, mRNA and protein expression levels of B‑cell lymphoma 2 apoptosis regulator (Bcl‑2) and Bcl‑2 associated protein X apoptosis regulator (Bax) were examined using RT‑qPCR and western blotting. The results demonstrated that miR‑320a expression was significantly increased in PCOS tissues compared with normal tissues. Moreover, miR‑320a was upregulated in insulin‑induced cells in a dose‑dependent manner. Inhibition of miR‑320a suppressed insulin‑induced cell viability and colony formation, and promoted apoptosis. Luciferase reporter assays demonstrated that PCGF1 was a target of miR‑320a. Additionally, PCGF1 overexpression inhibited cell viability and colony formation and promoted apoptosis. Additionally, the mRNA and protein levels of Bcl‑2 were inhibited by miR‑320a suppression and PCGF1 overexpression, while Bax expression was promoted by them in insulin‑induced cells. The results of the present study demonstrated that miR‑320a inhibition decreased insulin‑induced KGN cell proliferation and apoptosis by targeting PCGF1. These data indicated that miR‑320a may serve as a potential diagnostic biomarker for PCOS.

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October-2017
Volume 16 Issue 4

Print ISSN: 1791-2997
Online ISSN:1791-3004

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Spandidos Publications style
Yang L, Li Y, Wang X, Liu Y and Yang L: MicroRNA‑320a inhibition decreases insulin‑induced KGN cell proliferation and apoptosis by targeting PCGF1. Mol Med Rep 16: 5706-5712, 2017
APA
Yang, L., Li, Y., Wang, X., Liu, Y., & Yang, L. (2017). MicroRNA‑320a inhibition decreases insulin‑induced KGN cell proliferation and apoptosis by targeting PCGF1. Molecular Medicine Reports, 16, 5706-5712. https://doi.org/10.3892/mmr.2017.7270
MLA
Yang, L., Li, Y., Wang, X., Liu, Y., Yang, L."MicroRNA‑320a inhibition decreases insulin‑induced KGN cell proliferation and apoptosis by targeting PCGF1". Molecular Medicine Reports 16.4 (2017): 5706-5712.
Chicago
Yang, L., Li, Y., Wang, X., Liu, Y., Yang, L."MicroRNA‑320a inhibition decreases insulin‑induced KGN cell proliferation and apoptosis by targeting PCGF1". Molecular Medicine Reports 16, no. 4 (2017): 5706-5712. https://doi.org/10.3892/mmr.2017.7270