title: Surviving metabolic stress: of mice (squirrels) and men.
abstract: Understanding how cancer cells survive harsh environmental conditions may be fundamental to eradicating malignancies proven to be impervious to treatment. Nutrient and growth factor deprivation, hypoxia, and low pH create metabolic demands that require cellular adaptations to sustain energy levels. Protein synthesis is one of the most notable consumers of energy. Mounting evidence implicates exquisite control of protein synthesis as a survival mechanism for both normal and malignant cells. In this commentary, we discuss the role of protein synthesis in energy conservation in cancer and focus on elongation factor-2 kinase, a downstream component of the PI3K-AKT pathway that behaves as a critical checkpoint in energy consumption. .
authors.affiliation: Authors' Affiliations:Janssen R&D, LLC., Raritan, New Jersey; Department of Pharmacology, Penn State University College of Medicine; and Penn State Hershey Cancer Institute, Milton S. Hershey Medical Center, Hershey, Pennsylvania Whait@its.jnj.com.
authors.forename: William N
authors.initials: WN
authors.lastname: Hait
authors.affiliation: Authors' Affiliations:Janssen R&D, LLC., Raritan, New Jersey; Department of Pharmacology, Penn State University College of Medicine; and Penn State Hershey Cancer Institute, Milton S. Hershey Medical Center, Hershey, Pennsylvania.
authors.forename: Matthias
authors.initials: M
authors.lastname: Versele
authors.affiliation: Authors' Affiliations:Janssen R&D, LLC., Raritan, New Jersey; Department of Pharmacology, Penn State University College of Medicine; and Penn State Hershey Cancer Institute, Milton S. Hershey Medical Center, Hershey, PennsylvaniaAuthors' Affiliations:Janssen R&D, LLC., Raritan, New Jersey; Department of Pharmacology, Penn State University College of Medicine; and Penn State Hershey Cancer Institute, Milton S. Hershey Medical Center, Hershey, Pennsylvania.
authors.forename: Jin-Ming
authors.initials: JM
authors.lastname: Yang
mesh_terms: D055372:AMP-Activated Protein Kinases / Q000378:metabolism; D000818:Animals; D054736:Elongation Factor 2 Kinase / Q000378:metabolism*; D006801:Humans; D000076222:Mechanistic Target of Rapamycin Complex 1; D051379:Mice; D046912:Multiprotein Complexes / Q000378:metabolism; D009369:Neoplasms / Q000378:metabolism*; D019869:Phosphatidylinositol 3-Kinases / Q000378:metabolism; D012589:Sciuridae; D013312:Stress, Physiological; D058570:TOR Serine-Threonine Kinases / Q000378:metabolism
chemical_list: D055372:AMP-Activated Protein Kinases; D054736:Elongation Factor 2 Kinase; D000076222:Mechanistic Target of Rapamycin Complex 1; D046912:Multiprotein Complexes; D019869:Phosphatidylinositol 3-Kinases; D058570:TOR Serine-Threonine Kinases