The HSP90/Akt pathway may mediate artemether-induced apoptosis of Cal27 cells

FEBS Open Bio. 2019 Oct;9(10):1726-1733. doi: 10.1002/2211-5463.12711. Epub 2019 Aug 30.

Abstract

Tongue squamous cell carcinoma is the most common malignant tumor in oral and maxillofacial regions. Recent research has found that artemether can inhibit growth and induce apoptosis of cancer cells, although the mechanism is not clear. The present study aimed to explore the correlation between the HSP90/Akt pathway and artemether-induced apoptosis of Cal27 cells. A cell counting kit-8 and flow cytometry were used to detect the proliferation and apoptosis of Cal27 cells, respectively, mRNA expression was examined by quantitative RT-PCR, and protein expression was detected by western blotting. Our data revealed that artemether can inhibit growth and induce apoptosis of Cal27 cells. As the artemether concentration was increased, we observed downregulation of the expression of HSP90, p-Akt and p-mTOR in Cal27 cells, whereas the expression of Akt was not significantly changed. We also observed a time-dependent decrease in the expression of HSP90, p-Akt and p-mTOR during exposure to 0.1 mg·mL-1 artemether. In conclusion, the HSP90/Akt pathway may be involved in artemether-induced apoptosis of Cal27 cells.

Keywords: Akt; HSP90; apoptosis; artemether; tongue squamous cell carcinoma.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Apoptosis / drug effects*
  • Artemether / pharmacology*
  • Cell Proliferation / drug effects
  • Dose-Response Relationship, Drug
  • HSP90 Heat-Shock Proteins / genetics
  • HSP90 Heat-Shock Proteins / metabolism*
  • Humans
  • Proto-Oncogene Proteins c-akt / genetics
  • Proto-Oncogene Proteins c-akt / metabolism*
  • Signal Transduction / drug effects*
  • Structure-Activity Relationship
  • Tumor Cells, Cultured

Substances

  • HSP90 Heat-Shock Proteins
  • Artemether
  • Proto-Oncogene Proteins c-akt