Journal
CELL STRESS & CHAPERONES
Volume 21, Issue 4, Pages 553-562Publisher
SPRINGER
DOI: 10.1007/s12192-016-0687-3
Keywords
TRAP1; Apoptosis; Fatty liver; Cancer stem cells; Warburg effect
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Funding
- Basic Science Research Program through National Research Foundation of Korea (NRF) - Ministry of Science, ICT and Future Planning [NRF-2014R1A1A1006961]
- National Research Foundation of Korea [2014R1A1A1006961] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
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Tumor necrosis factor receptor-associated protein 1 (TRAP1), a member of the HSP90 family, controls a variety of physiological functions, including cell proliferation, differentiation, and survival. Most studies have been devoted to understanding the anti-apoptotic roles of TRAP1 in cancer and targeting it for tumor control in clinical settings. Additionally, we have identified a new role for TRAP1 in regulation of liver regeneration after partial hepatectomy in TRAP1 transgenic mice and cellular proliferation in TRAP1-overexpressing cells, via mitochondrial alterations. Moreover, recent works have indicated a role for TRAP1 in the regulation of cancer stem cells (CSCs) as well as a metabolic switch between mitochondrial respiration and aerobic glycolysis called as Warburg effect. This review discusses the implications of TRAP1 action for both metabolism and the regulation of CSCs.
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