Droxinostat sensitizes human colon cancer cells to apoptotic cell death via induction of oxidative stress

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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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Huang, Y., Yang, W., Zeng, H., Hu, C., Zhang, Y., Ding, N., … Kuang, B. (2018). Droxinostat sensitizes human colon cancer cells to apoptotic cell death via induction of oxidative stress. Cellular and Molecular Biology Letters, 23(1). https://doi.org/10.1186/s11658-018-0101-5

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