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Michelia compressa-Derived Santamarine Inhibits Oral Cancer Cell Proliferation via Oxidative Stress-Mediated Apoptosis and DNA Damage

Authors :
Hsin-I Lu
Kuan-Liang Chen
Ching-Yu Yen
Chung-Yi Chen
Tsu-Ming Chien
Chih-Wen Shu
Yu-Hsuan Chen
Jiiang-Huei Jeng
Bing-Hung Chen
Hsueh-Wei Chang
Source :
Pharmaceuticals, Vol 17, Iss 2, p 230 (2024)
Publication Year :
2024
Publisher :
MDPI AG, 2024.

Abstract

The anti-oral cancer effects of santamarine (SAMA), a Michelia compressa var. compressa-derived natural product, remain unclear. This study investigates the anticancer effects and acting mechanism of SAMA against oral cancer (OC-2 and HSC-3) in parallel with normal (Smulow–Glickman; S-G) cells. SAMA selectively inhibits oral cancer cell viability more than normal cells, reverted by the oxidative stress remover N-acetylcysteine (NAC). The evidence of oxidative stress generation, such as the induction of reactive oxygen species (ROS) and mitochondrial superoxide and the depletion of mitochondrial membrane potential and glutathione, further supports this ROS-dependent selective antiproliferation. SAMA arrests oral cancer cells at the G2/M phase. SAMA triggers apoptosis (annexin V) in oral cancer cells and activates caspases 3, 8, and 9. SAMA enhances two types of DNA damage in oral cancer cells, such as γH2AX and 8-hydroxy-2-deoxyguanosine. Moreover, all of these anticancer mechanisms of SAMA are more highly expressed in oral cancer cells than in normal cells in concentration and time course experiments. These above changes are attenuated by NAC, suggesting that SAMA exerts mechanisms of selective antiproliferation that depend on oxidative stress while maintaining minimal cytotoxicity to normal cells.

Details

Language :
English
ISSN :
14248247
Volume :
17
Issue :
2
Database :
Directory of Open Access Journals
Journal :
Pharmaceuticals
Publication Type :
Academic Journal
Accession number :
edsdoj.445a154747194cfb9761eb6a52c8163c
Document Type :
article
Full Text :
https://doi.org/10.3390/ph17020230