Title |
Droxinostat sensitizes human colon cancer cells to apoptotic cell death via induction of oxidative stress
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Published in |
Cellular & Molecular Biology Letters, July 2018
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DOI | 10.1186/s11658-018-0101-5 |
Pubmed ID | |
Authors |
Ying Huang, Wuping Yang, Huihong Zeng, Chuan Hu, Yaqiong Zhang, Nanhua Ding, Guangqin Fan, Lijian Shao, Bohai Kuang |
Abstract |
Upregulation of histone acetylation plays a critical role in the dysregulation of transcription. It alters the structure of chromatin, which leads to the onset of cancer. Histone deacetylase inhibitors may therefore be a promising way to limit cancer progression. In this study, we examined the effects of droxinostat on the growth of HT-29 colon cancer cells. Our results show that droxinostat effectively inhibited cell growth and colony-forming ability by inducing cellular apoptosis and ROS production in HT-29 cells. Notably, the apoptotic inhibitor Z-VAD-FMK significantly decreased the levels of cellular apoptosis and the antioxidant γ-tocotrienol (GT3) significantly decreased ROS production induced by droxinostat treatment. Z-VAD-FMK and GT3 also partially reversed the negative growth effects of droxinstat on HT-29 cells. GT3 treatment decreased cellular apoptosis and increased colony-forming ability upon droxinostat administration. Z-VAD-FMK treatment also partially decreased droxinostat-induced ROS production. Our findings suggest that the effects of droxinostat on colon cancer cells are mediated by the induction of oxidative stress and apoptotic cell death. |
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Unknown | 5 | 38% |