Molecular biology reports · 2025
Excavatolide E triggers oxidative stress-associated apoptosis and DNA damage to inhibit bladder cancer cell proliferation.
СтатьяНазвание и аннотация: Перевод в очереди
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Yang Che-Wei, Yen Chia-Hung, Chien Tsu-Ming, Yu Szu-Yin, Chang Fang-Rong, Sheu Jyh-Horng, Chang Hsueh-Wei
Аннотация
BACKGROUND: Excavatolide E (EXCE), a biocompound extracted from the gorgonian octocoral Briareum excavatum, has received limited attention for its anticancer properties, especially in the context of bladder cancer.
METHODS: Cell viability, flow cytometry, and Western blotting were performed to assess the antiproliferative effects and mechanisms against bladder cancer cells.
RESULTS: In the present study, the impacts and mechanisms of EXCE's antiproliferative effects on bladder cancer cells were assessed, along with its impacts on normal cells. EXCE selectively inhibited proliferation of bladder cancer cells, as compared to normal cells, i.e., selectivity index > 2, and induced greater oxidative stress in bladder cancer cells than normal cells, regarding the induction of cellular and mitochondrial ROS, as well as the depletion of mitochondrial membrane potential. Moreover, EXCE triggered higher levels of apoptosis, both extrinsic and intrinsic caspase activation, and DNA damage in bladder cancer cells than in normal cell; these EXCE-triggered antiproliferative mechanisms were alleviated by N-acetylcysteine (NAC), a ROS inhibitor.
CONCLUSION: Therefore, EXCE's antiproliferative activity offers a promising therapeutic approach for targeting bladder cancer cells by modulating oxidative stress, while preserving the safety of normal cells.
METHODS: Cell viability, flow cytometry, and Western blotting were performed to assess the antiproliferative effects and mechanisms against bladder cancer cells.
RESULTS: In the present study, the impacts and mechanisms of EXCE's antiproliferative effects on bladder cancer cells were assessed, along with its impacts on normal cells. EXCE selectively inhibited proliferation of bladder cancer cells, as compared to normal cells, i.e., selectivity index > 2, and induced greater oxidative stress in bladder cancer cells than normal cells, regarding the induction of cellular and mitochondrial ROS, as well as the depletion of mitochondrial membrane potential. Moreover, EXCE triggered higher levels of apoptosis, both extrinsic and intrinsic caspase activation, and DNA damage in bladder cancer cells than in normal cell; these EXCE-triggered antiproliferative mechanisms were alleviated by N-acetylcysteine (NAC), a ROS inhibitor.
CONCLUSION: Therefore, EXCE's antiproliferative activity offers a promising therapeutic approach for targeting bladder cancer cells by modulating oxidative stress, while preserving the safety of normal cells.