NDLI: SIRT3 participates in glucose metabolism interruption and apoptosis induced by BH3 mimetic S1 in ovarian cancer cells.

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SIRT3 participates in glucose metabolism interruption and apoptosis induced by BH3 mimetic S1 in ovarian cancer cells.

Content Provider	Semantic Scholar
Author	Xiang, Xi-yan Kang, Jin-song Yang, Xiao-chun Su, Jing Wu, Yao Yan, Xiao-Yu Xue, Ya-Nan Liu, Yu-He Yu, Chun-yan Zhang, Zhi-chao Sun, Liankun
Copyright Year	2016
Abstract	The Bcl-2 antiapoptotic proteins are important cancer therapy targets; however, their role in cancer cell metabolism remains unclear. We found that the BH3-only protein mimetic S1, a novel pan Bcl-2 inhibitor, simultaneously interrupted glucose metabolism and induced apoptosis in human SKOV3 ovarian cancer cells, which was related to the activation of SIRT3, a stress-responsive deacetylase. S1 interrupted the cellular glucose metabolism mainly through causing damage to mitochondrial respiration and inhibiting glycolysis. Moreover, S1 upregulated the gene and protein expression of SIRT3, and induced the translocation of SIRT3 from the nucleus to mitochondria. SIRT3 silencing reversed the effects of S1 on glucose metabolism and apoptosis through increasing the level of HK-II localized to the mitochondria, while a combination of the glycolysis inhibitor 2-DG and S1 intensified the cytotoxicity through further upregulation of SIRT3 expression. This study underscores an essential role of SIRT3 in the antitumor effect of Bcl-2 inhibitors in human ovarian cancer through regulating both metabolism and apoptosis. The manipulation of Bcl-2 inhibitors combined with the use of classic glycolysis inhibitors may be rational strategies to improve ovarian cancer therapy.
Starting Page	114
Ending Page	115
Page Count	2
File Format	PDF HTM / HTML
Alternate Webpage(s)	https://www.spandidos-publications.com/10.3892/ijo.2016.3552/download
PubMed reference number	27277143v1
Alternate Webpage(s)	https://doi.org/10.3892/ijo.2016.3552
DOI	10.3892/ijo.2016.3552
Journal	International journal of oncology
Volume Number	49
Issue Number	2
Language	English
Access Restriction	Open
Subject Keyword	Antiapoptotic Agent Apoptosis BCL2 gene Cell Nucleus Deacetylase Deoxyglucose Glycolysis Inhibition Malignant neoplasm of ovary Mitochondria Neoplasms Up-Regulation (Physiology) cancer cell glucose metabolism ovarian neoplasm protein expression
Content Type	Text
Resource Type	Article

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