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Sinularin induces oxidative stress-mediated G2/M arrest and apoptosis in oral cancer cells
Yung-Ting Chang1,2, Chang-Yi Wu3, Jen-Yang Tang4,5,6
1Doctoral Degree Program in Marine Biotechnology, National Sun Yat-sen University, Kaohsiung, 80424, Taiwan.
Abstract:
Soft corals-derived natural product, sinularin, was antiproliferative against some cancers but its effect and detailed mechanism on oral cancer cells remain unclear. The subject of this study is to examine the antioral cancer effects and underlying detailed mechanisms in terms of cell viability, oxidative stress, cell cycle analysis, and apoptosis analyses. In MTS assay, sinularin dose-responsively decreased cell viability of three oral cancer cells (Ca9-22, HSC-3, and CAL 27) but only little damage to oral normal cells (HGF-1). This cell killing effect was rescued by the antioxidant N-acetylcysteine (NAC) pretreatment. Abnormal cell morphology and induction of reactive oxygen species (ROS) were found in sinularin-treated oral cancer Ca9-22 cells, however, NAC pretreatment also recovered these changes. Sinularin arrested the Ca9-22 cells at G2/M phase and dysregulated the G2/M regulatory proteins such as cdc2 and cyclin B1. Sinularin dose-responsively induced apoptosis on Ca9-22 cells in terms of flow cytometry (annexin V and pancaspase analyses) and western blotting (caspases 3, 8, 9) and poly (ADP-ribose) polymerase (PARP). These apoptotic changes of sinularin-treated Ca9-22 cells were rescued by NAC pretreatment. Taken together, sinularin induces oxidative stress-mediated antiproliferation, G2/M arrest, and apoptosis against oral cancer cells and may be a potential marine drug for antioral cancer therapy.
Insights
Sinularin, a marine natural product, effectively reduces oral cancer cell viability and induces apoptosis by increasing oxidative stress. This compound shows potential as a marine drug for oral cancer therapy.
Area of Science:
- Marine natural products
- Cancer research
- Molecular pharmacology
Background:
- Sinularin, derived from soft corals, exhibits antiproliferative effects against certain cancers.
- The precise mechanisms of sinularin's action on oral cancer remain largely unelucidated.
- Understanding sinularin's impact on oral cancer is crucial for developing novel therapeutic strategies.
Purpose of the Study:
- To investigate the anti-oral cancer effects of sinularin.
- To elucidate the detailed mechanisms, including effects on cell viability, oxidative stress, cell cycle, and apoptosis.
- To evaluate sinularin's potential as a marine-derived therapeutic agent for oral cancer.
Main Methods:
- Cell viability assessed using MTS assay on oral cancer and normal cell lines.
- Reactive oxygen species (ROS) generation and cell morphology changes observed.
- Cell cycle progression analyzed via flow cytometry.
- Apoptosis induction evaluated through flow cytometry and Western blotting.
Main Results:
- Sinularin dose-dependently decreased oral cancer cell viability with minimal impact on normal cells.
- Sinularin treatment induced oxidative stress and G2/M cell cycle arrest in oral cancer cells.
- Apoptosis was significantly induced by sinularin, involving caspase activation and PARP cleavage.
- Antioxidant N-acetylcysteine (NAC) pretreatment rescued sinularin-induced effects, confirming the role of oxidative stress.
Conclusions:
- Sinularin exhibits significant anti-oral cancer activity by mediating antiproliferation, G2/M arrest, and apoptosis.
- Oxidative stress is a key mechanism underlying sinularin's cytotoxic effects on oral cancer cells.
- Sinularin represents a promising marine-derived compound for potential oral cancer treatment.
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