NDLI: Blockage of glutaminolysis enhances the sensitivity of ovarian cancer cells to PI3K/mTOR inhibition involvement of STAT3 signaling

Content Provider	Springer Nature Link
Author	Guo, Lili Zhou, Bo Liu, Zhengqing Xu, Ying Lu, Hao Xia, Meng Guo, Ensong Shan, Wanying Chen, Gang Wang, Changyu
Copyright Year	2016
Abstract	The PI3K/Akt/mTOR axis in ovarian cancer is frequently activated and implicated in tumorigenesis. Specific targeting of this pathway is therefore an attractive therapeutic approach for ovarian cancer. However, ovarian cancer cells are resistant to PP242, a dual inhibitor of mTORC1 and mTORC2. Interestingly, blockage of GLS1 with a selective inhibitor, CB839, or siRNA dramatically sensitized the PP242-induced cell death, as evident from increased PARP cleavage. The anti-cancer activity of CB-839 and PP242 was abrogated by the addition of the TCA cycle product α-ketoglutarate, indicating the critical function of GLS1 in ovarian cancer cell survival. Finally, glutaminolysis inhibition activated apoptosis and synergistically sensitized ovarian cancer cells to priming with the mTOR inhibitor PP242. GLS1 inhibition significantly reduced phosphorylated STAT3 expression in ovarian cancer cells. These findings show that targeting glutamine addiction via GLS1 inhibition offers a potential novel therapeutic strategy to overcome resistance to PI3K/Akt/mTOR inhibition.
Starting Page	11007
Ending Page	11015
Page Count	9
File Format	PDF
ISSN	10104283
Journal	Tumor Biology
Volume Number	37
Issue Number	8
e-ISSN	14230380
Language	English
Publisher	Springer Netherlands
Publisher Date	2016-02-19
Publisher Place	Dordrecht
Access Restriction	Subscribed
Subject Keyword	Glutaminase1 GLS1 Metabolic reprogramming Ovarian cancer Drug resistance Cancer Research
Content Type	Text
Resource Type	Article
Subject	Medicine Cancer Research

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