title: Molecular chaperones regulate p53 and suppress senescence programs.
abstract: Many types of cancer cells constitutively express major molecular chaperones at high levels. Recent findings demonstrate that specific depletion of individual chaperones, including various members of the Hsp70 family, small heat shock proteins, or VCP/p97, leads to activation of p53 pathway and subsequently triggers cellular senescence. Here, we discuss a possibility that in cancer cells high levels of chaperones serve to keep the p53 signaling under control, thus allowing cancer cells to evade the default senescence and form tumors.
authors.affiliation: Department of Biochemistry, Boston University Medical School, 715 Albany Street, K323, Boston, MA 02118, United States. sherma1@bu.edu
authors.forename: Michael Y
authors.initials: MY
authors.lastname: Sherman
authors.forename: Michael
authors.initials: M
authors.lastname: Sherman
authors.forename: Vladimir
authors.initials: V
authors.lastname: Gabai
authors.forename: Cornelia
authors.initials: C
authors.lastname: O'Callaghan
authors.forename: Julia
authors.initials: J
authors.lastname: Yaglom
mesh_terms: D000818:Animals; D016922:Cellular Senescence; D006801:Humans; D018832:Molecular Chaperones / Q000378:metabolism*; D009369:Neoplasms / Q000378:metabolism / Q000473:pathology*; D016159:Tumor Suppressor Protein p53 / Q000235:genetics / Q000378:metabolism*
chemical_list: D018832:Molecular Chaperones; D016159:Tumor Suppressor Protein p53