The caspase 3-dependent apoptotic effect of pycnogenol in human oral squamous cell carcinoma HSC-3 cells
In-Hyoung Yang1, Ji-Ae Shin1, Lee-Han Kim1
1Department of Oral Pathology, School of Dentistry, and Institute of Oral Bioscience, Chonbuk National University, Jeonju 561-756, Korea.
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.
Insights
Pycnogenol effectively combats oral cancer by inducing apoptosis in cancer cells. This natural compound shows promise for future chemoprevention and chemotherapy strategies against oral squamous cell carcinoma.
Area of Science:
- Oncology
- Molecular Biology
- Pharmacology
Background:
- Oral squamous cell carcinoma (OSCC) is a significant global health concern.
- Identifying novel therapeutic agents for OSCC chemoprevention and chemotherapy is crucial.
Purpose of the Study:
- To investigate the apoptotic effects of Pycnogenol on human oral cancer cells (HSC-3).
- To elucidate the molecular mechanisms underlying Pycnogenol's anti-cancer activity.
Main Methods:
- Cell viability assays were performed on HSC-3 cells treated with Pycnogenol.
- Apoptosis markers, including cleaved poly (ADP-ribose) polymerase and caspase 3, were analyzed.
- Protein levels of Bcl-2 family members and reactive oxygen species (ROS) production were assessed.
Main Results:
- Pycnogenol significantly inhibited HSC-3 cell viability and neoplastic cell transformation.
- Pycnogenol induced caspase-dependent apoptosis in a dose-dependent manner.
- Pycnogenol increased Bak protein stability and induced ROS generation, which was partially blocked by N-acetyl-l-cysteine.
Conclusions:
- Pycnogenol demonstrates potent anti-cancer properties against human oral squamous cell carcinoma cells.
- The mechanism involves caspase-dependent apoptosis, modulation of Bak protein, and ROS production.
- Pycnogenol holds potential as a therapeutic agent for oral cancer chemoprevention or chemotherapy.
Related Concept Videos
Caspases
The Intrinsic Apoptotic Pathway
Apoptosis


