Sodium butyrate promotes apoptosis in breast cancer cells through reactive oxygen species (ROS) formation and mitochondrial impairment

Lipids in Health and Disease

Research

Banafsheh Safizadeh¹  Narges Khademian²  Ameinh Hosseini²  Masoumeh Tavakoli-Yaraki²  Zahra Shahsavari³  Vahid Salimi⁴ 

[1] Department of Biochemistry, Faculty of Medicine, Birjand University of Medical Sciences, Birjand, Iran;Department of Biochemistry, School of Medicine, Iran University of Medical Sciences, Tehran, Iran;Department of Laboratory Medicine, Faculty of Paramedical Sciences, Shaheed Beheshti University of Medical Sciences, Tehran, Iran;Department of Virology, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran;

关键词: Sodium butyrate;    Apoptosis;    Cell cycle;    Reactive oxygen species;    Caspase;    Mitochondrial membrane potential (Δψm);   

DOI  :  10.1186/s12944-017-0593-4

 received in 2017-05-14, accepted in 2017-10-11,  发布年份 2017

来源: Springer

【 摘 要 】

BackgroundSodium butyrate (NaBu) is a short-chain fatty acid which serves as a histon deacetylase inhibitor and has received considerable interest as a possible regulator of cancer cell death. The regulatory effect of NaBu on cancer cell growth or death has yet to be illustrated in many cancers including breast cancer. This study is aimed to elucidate the possible effect of NaBu on regulation of breast cancer growth and apoptosis.MethodsThe cytotoxic effect of NaBu on the growth of breast cancer cells (MCF-7 and MDA-MB-468) and normal breast cells (MCF-10A) was determined using MTT assay. Annexin-V-FITC staining and PI staining were performed to detect apoptosis and cell cycle distribution using Flow cytometry, the level of mitochondrial membrane potential (Δψm), Reactive oxygen species (ROS)formation and caspase activity were determined accordingly.ResultsBased on our data, NaBu induced a dose and time-dependent cell toxicity in breast cancer cells which was related to the cell cycle arrest and induction of apoptosis. The impact of NaBu on MCF-10A cell toxicity, cell cycle distribution and apoptosis was inconsiderable. NaBu-elicited apoptosis was accompanied by the elevated level of ROS, increased caspase activity and reduced mitochondrial membrane potential (Δψm) in MCF-7 and MDA-MB-468 cells and with no effect on the above mentioned factors in MCF-10A cells.ConclusionsOur study provided insight in to the role of NaBu on the regulation of breast cancer cell growth and lighten up the pro-apoptotic activity of NaBu.

【 授权许可】

CC BY   
© The Author(s). 2017