ArticleDoklady. Biochemistry and biophysics2025
The Role of TRPM2 Channel in Doxorubicin-induced Cell Damage in Laryngeal Squamous Cancer Cells.
Article in Doklady. Biochemistry and biophysics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Sinapic Acid Reduces Hypoxia-Induced Cell Damage in Hep-2 Cells by Regulating TRPM2 Channel Activation.Journal of biochemical and molecular toxicology · 2026Article
- TRPM2 Channel Involvement in the Hesperidin-Mediated Potentiation of Cisplatin's Antitumor Action in Laryngeal Carcinoma Cells.International journal of molecular sciences · 2026Article
- New Anti-Cancer Impact of Cerium Oxide, Lithium, and Sn-38 Synergy via DNA Methylation-Mediated Reduction of MMP-2 and Modulation of the PI3K/Akt/mTOR Pathway.Pharmaceuticals (Basel, Switzerland) · 2025Article
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Authors and funding
5 authors.
Funding
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Abstract
Laryngeal squamous cell carcinoma is a common type of head and neck cancer. This study investigated the role of the TRPM2 channel in doxorubicin (DOX)-induced cell damage in human laryngeal squamous cancer cells (Hep-2). Cells were exposed to various DOX concentrations and the appropriate dose was found. Then, TRPM2 antagonist ACA was treated. At the end of the study, cell viability test, Western blot and oxidative stress and inflammatory markers were examined. The results showed that TRPM2 channel expression increased with DOX administration, and DOX incubation in cells caused an increase in ROS, MDA, IL-1β, IL-6, and TNF-α levels, while GSH and GSH-Px levels decreased. Concurrent treatment with ACA attenuated these effects and reduced oxidative stress and inflammation. In addition, DOX-induced apoptosis markers including Casp-3, Casp-8, Casp-9, p53, and Bax were elevated, while Bcl-2 levels were decreased; ACA treatment reversed these changes. The study demonstrated that DOX treatment significantly enhances TRPM2 channel activation and ROS production in Hep-2 cells, thereby initiating apoptotic pathways that lead to cell death. Consequently, targeting the TRPM2 channel may represent a promising therapeutic strategy for treating laryngeal cancer.
Indexed as
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.