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Published on: August 23, 2024
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.
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.
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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