title: Dissecting the Dual Role of AMPK in Cancer: From Experimental to Human Studies.
abstract: The precise role of 5'AMP-activated kinase (AMPK) in cancer and its potential as a therapeutic target is controversial. Although it is well established that activation of this energy sensor inhibits the main anabolic processes that sustain cancer cell proliferation and growth, AMPK activation can confer on cancer cells the plasticity to survive under metabolic stress such as hypoxia and glucose deprivation, which are commonly observed in fast growing tumors. Thus, AMPK is referred to as both a "conditional" tumor suppressor and "contextual" oncogene. To add a further layer of complexity, AMPK activation in human cancer tissues and its correlation with tumor aggressiveness and progression appears to vary in different contexts. The current review discusses the different faces of this metabolic regulator, the therapeutic implications of its modulation, and provides an overview of the most relevant data available on AMPK activation and AMPK-activating drugs in human studies.
authors.affiliation: Department of Medical Oncology, Dana-Farber Cancer Institute, Brigham and Women's Hospital, Boston, Massachusetts. Department of Pathology, Dana-Farber Cancer Institute, Brigham and Women's Hospital, Boston, Massachusetts.
authors.forename: Giorgia
authors.initials: G
authors.lastname: Zadra
authors.affiliation: Department of Epidemiology, Harvard School of Public Health, Boston, Massachusetts. Channing Division of Network Medicine, Brigham and Women's Hospital/Harvard Medical School Boston, Massachusetts.
authors.forename: Julie L
authors.initials: JL
authors.lastname: Batista
authors.affiliation: Department of Medical Oncology, Dana-Farber Cancer Institute, Brigham and Women's Hospital, Boston, Massachusetts. Department of Pathology, Dana-Farber Cancer Institute, Brigham and Women's Hospital, Boston, Massachusetts. The Broad Institute, Cambridge, Massachusetts. Division of Cancer Studies, King's College London, United Kingdom. massimo_loda@dfci.harvard.edu.
authors.forename: Massimo
authors.initials: M
authors.lastname: Loda
mesh_terms: D055372:AMP-Activated Protein Kinases / Q000037:antagonists & inhibitors / Q000378:metabolism*; D000818:Animals; D000970:Antineoplastic Agents / Q000378:metabolism / Q000627:therapeutic use; D015687:Cell Hypoxia; D049109:Cell Proliferation; D016147:Genes, Tumor Suppressor; D006801:Humans; D009369:Neoplasms / Q000188:drug therapy / Q000378:metabolism*; D009857:Oncogenes; D013312:Stress, Physiological
chemical_list: D000970:Antineoplastic Agents; D055372:AMP-Activated Protein Kinases