Molecular chaperones regulate p53 and suppress senescence programs.
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.
Sherman
Michael Y
MY
Department of Biochemistry, Boston University Medical School, 715 Albany Street, K323, Boston, MA 02118, United States. sherma1@bu.edu
Sherman
Michael
M
Gabai
Vladimir
V
O'Callaghan
Cornelia
C
Yaglom
Julia
J
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*
D018832:Molecular Chaperones; D016159:Tumor Suppressor Protein p53