期刊
AUTOPHAGY
卷 11, 期 8, 页码 1198-1208出版社
TAYLOR & FRANCIS INC
DOI: 10.1080/15548627.2015.1053680
关键词
autophagy; cancer; glutaminolysis; MTOR; prolyl hydroxylases; ROS; alpha-ketoglutarate
类别
资金
- Institut National de la Sante et de la Recherche Medicale INSERM
- Universite de Bordeaux
- Fondation pour la Recherche Medicale
- Conseil Regional d'Aquitaine
- Fondation ARC pour la Recherche sur le Cancer
- SIRIC-BRIO
- Institut Europeen de Chimie et Biologie
- Institut Bergonie
- Ligue contre le Cancer - Comite de la Gironde
- Institut National du Cancer
The remarkable metabolic differences between cancer cells and normal cells result in the potential for targeted cancer therapy. The upregulation of glutaminolysis provides energetic advantages to cancer cells. The recently described link between glutaminolysis and autophagy, mediated by MTORC1, may constitute an attractive target for therapeutic strategies. A combination of therapies targeting simultane-ously cell signaling, cancer metabolism, and autophagy can solve therapy resistance and tumor relapse problems, commonly observed in patients treated with most of the current targeted therapies. In this review we summarize the mechanistic link between glutaminolysis and autophagy, and discuss the impacts of these processes on cancer progression and the potential for therapeutic intervention.
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