MiR-122 partly mediates the ochratoxin A-induced GC-2 cell apoptosis

Toxicol In Vitro. 2015 Dec 25;30(1 Pt B):264-73. doi: 10.1016/j.tiv.2015.10.011. Epub 2015 Oct 26.

Abstract

Ochratoxin A (OTA) is a mycotoxin which has been shown to be nephrotoxic, hepatotoxic, and immunotoxic to animals, and mainly exists in the mildew grain. MicroRNAs (miRNAs) regulate a wide variety of cellular processes. However, the toxic effects of OTA on the germ cell and whether miRNAs mediate the effects of OTA-induced GC-2 cell apoptosis are still not clear. In the present study, OTA treatment resulted in a dose-dependent increase apoptosis in GC-2 cells. MiR-122 was increased in the OTA-treated GC-2 cells. It showed that Bcl-w was down-regulated after OTA treatment, and caspase-3 was obviously activated. Cyclin G1 (CCNG1) was significantly decreased, and inversely the expression of p53 was increased. Inhibition of miR-122 partly relieved the OTA-induced GC-2 cell apoptosis. These results indicate that OTA induces GC-2 cell apoptosis by causing the increase of caspase-3 activity and that miR-122 partly mediates the OTA-induced cell apoptosis.

Keywords: Cell apoptosis; GC-2 cell; Ochratoxin A; miR-122.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Apoptosis / drug effects*
  • Base Sequence
  • Caspase 3 / metabolism
  • Cells, Cultured
  • Cyclin G1 / physiology
  • Dose-Response Relationship, Drug
  • Humans
  • Male
  • MicroRNAs / physiology*
  • Molecular Sequence Data
  • Ochratoxins / toxicity*
  • Spermatocytes / drug effects*
  • Spermatocytes / physiology
  • Tumor Suppressor Protein p53 / physiology

Substances

  • CCNG1 protein, human
  • Cyclin G1
  • MIRN122 microRNA, human
  • MicroRNAs
  • Ochratoxins
  • Tumor Suppressor Protein p53
  • ochratoxin A
  • Caspase 3