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Dihydroartemisinin Induces ER Stress-Mediated Apoptosis in Human Tongue Squamous Carcinoma by Regulating ROS
Qun Zhou1, Fangfei Ye1, Jiaxuan Qiu1
1Department of Oral and Maxillofacial Surgery, The First Affiliated Hospital of Nanchang University, Nanchang, Jiangxi, P.R. China.
Background:
Tongue squamous cell carcinoma is a fatal disease characterized by high invasion and early metastasis. Dihydroartemisinin, an antimalarial drug with multiple biological activities, is reported to be a potential anti-cancer agent.
Objective:
This study aimed to evaluate the antitumor effect of Dihydroartemisinin on tongue squamous cell carcinoma cells, and to identify the underlying mechanisms of Dihydroartemisinin-induced cell apoptosis.
Methods:
Here, Cell Counting Kit 8 assay and colony formation assay were conducted to study cell proliferation. Annexin V-FITC/propidium iodide staining and western blot analysis were performed to analyze cell apoptosis. DCFHDA probe was used to measure the generation of cellular reactive oxygen species. Endoplasmic reticulum stress activation was also determined via western blot analysis.
Results:
The results showed that Dihydroartemisinin substantially inhibited cell proliferation and induced cell apoptosis in vivo. Moreover, reactive oxygen species production and endoplasmic reticulum stress activation were both observed after stimulation with Dihydroartemisinin. However, the reactive oxygen species inhibitor N-acetylcysteine significantly alleviated Dihydroartemisinin-induced endoplasmic reticulum stress and apoptosis.
Conclusion:
These results imply that Dihydroartemisinin induced cell apoptosis by triggering reactive oxygen speciesmediated endoplasmic reticulum stress in CAL27 cells. In addition, Dihydroartemisinin might be an effective drug for tongue squamous cell carcinoma therapy.
Insights
Dihydroartemisinin effectively inhibits tongue squamous cell carcinoma (TSCC) by inducing apoptosis. This occurs through reactive oxygen species-mediated endoplasmic reticulum stress, suggesting its potential as a TSCC therapy.
Area of Science:
- Oncology
- Pharmacology
- Cell Biology
Background:
- Tongue squamous cell carcinoma (TSCC) is aggressive, marked by high invasion and metastasis.
- Dihydroartemisinin (DHA), an antimalarial, shows promise as an anti-cancer agent.
- Understanding DHA's anti-cancer mechanisms is crucial for therapeutic development.
Purpose of the Study:
- To assess the antitumor effects of Dihydroartemisinin on TSCC cells.
- To elucidate the molecular mechanisms behind Dihydroartemisinin-induced apoptosis in TSCC.
- To investigate the role of reactive oxygen species and endoplasmic reticulum stress in DHA's action.
Main Methods:
- Cell Counting Kit 8 and colony formation assays for proliferation.
- Annexin V-FITC/propidium iodide staining and Western blot for apoptosis.
- DCFHDA probe and Western blot for reactive oxygen species and endoplasmic reticulum stress.
Main Results:
- Dihydroartemisinin significantly inhibited TSCC cell proliferation and induced apoptosis.
- DHA treatment increased reactive oxygen species production and endoplasmic reticulum stress.
- N-acetylcysteine reversed DHA-induced endoplasmic reticulum stress and apoptosis.
Conclusions:
- Dihydroartemisinin induces TSCC cell apoptosis via reactive oxygen species-mediated endoplasmic reticulum stress.
- DHA demonstrates potential as a therapeutic agent for tongue squamous cell carcinoma.
- Targeting oxidative stress and ER stress pathways may enhance Dihydroartemisinin efficacy.
