ArticleJournal of clinical biochemistry and nutrition2016
The caspase 3-dependent apoptotic effect of pycnogenol in human oral squamous cell carcinoma HSC-3 cells.
Article in Journal of clinical biochemistry and nutrition, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 16 citations in OpenAlex.
- Role of Phytoconstituents in Cancer Treatment: A Review.Recent advances in food, nutrition & agriculture · 2024Review
- Bone marrow mesenchymal stem cellsderived exosomes stabilize atherosclerosis through inhibiting pyroptosis.BMC cardiovascular disorders · 2023Article
- Natural Products as Anticancer Agents: Current Status and Future Perspectives.Molecules (Basel, Switzerland) · 2022Review
- Protective Effect of Pycnogenol against Methotrexate-Induced Hepatic, Renal, and Cardiac Toxicity: An In Vivo Study.Pharmaceuticals (Basel, Switzerland) · 2022Article
- AnTurkish journal of pharmaceutical sciences · 2020Article
- Apoptosis induced by methanol extract of Potentilla discolor in human mucoepidermoid carcinoma cells through STAT3/PUMA signaling axis.Molecular medicine reports · 2018Article
- Does Notch play a tumor suppressor role across diverse squamous cell carcinomas?Cancer medicine · 2016Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In the present study, the apoptotic effect of pycnogenol and its molecular mechanism in human oral squamous cell carcinoma HSC-3 cells were investigated. Pycnogenol significantly inhibited the viability of HSC-3 cells and suppressed neoplastic cell transformation in HSC-3 cells and TPA-treated JB6 cells. It caused caspase-dependent apoptosis evidenced by the increase in cleaved poly (ADP-ribose) polymerase and caspase 3 in a dose-dependent manner. Pycnogenol increased Bak protein by enhancing its protein stability whereas other Bcl-2 family members were not altered. In addition, the treatment with pycnogenol led to the production of reactive oxygen species and N-acetyl-l-cysteine almost blocked pycnogenol-induced reactive oxygen species generation. Taken together, these findings suggest that pycnogenol may be a potential candidate for the chemoprevention or chemotherapy of human oral cancer.
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