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

Jianhua Wu1, Lei Li2, Yiting Wang3

  • 1Department of Periodontology, The Affiliated Stomatological Hospital of Kunming Medical University, Kunming, China.

FEBS Open Bio
|August 4, 2019
PubMed

Insights

Artemether inhibits tongue cancer cell growth and induces apoptosis. This study suggests the HSP90/Akt pathway is involved in artemether

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Tongue squamous cell carcinoma is a prevalent oral malignancy.
  • Artemether shows potential in inhibiting cancer cell growth and inducing apoptosis, but its mechanism remains unclear.

Purpose of the Study:

  • To investigate the role of the Heat Shock Protein 90 (HSP90)/Akt signaling pathway in artemether-induced apoptosis of Cal27 tongue cancer cells.

Main Methods:

  • Cell Counting Kit-8 assay for proliferation.
  • Flow cytometry for apoptosis detection.
  • Quantitative RT-PCR and Western blotting for gene and protein expression analysis.

Main Results:

  • Artemether inhibited Cal27 cell proliferation and induced apoptosis.
  • Increased artemether concentration led to decreased expression of HSP90, phosphorylated Akt (p-Akt), and phosphorylated mTOR (p-mTOR).
  • A time-dependent decrease in HSP90, p-Akt, and p-mTOR was observed with artemether treatment.

Conclusions:

  • The HSP90/Akt pathway is implicated in artemether-mediated apoptosis of Cal27 cells.
  • Findings suggest a potential therapeutic mechanism for artemether in tongue cancer treatment.

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