title: Cannibalism, cell survival, and endocrine resistance in breast cancer.
abstract: Breast cancer cells often respond to an endocrine therapy by altering expression of specific estrogen-responsive genes and inducing autophagy, a cannibalistic lysosomal pathway. Autophagy eliminates damaged or other organelles, allowing the recovery of the energy stored in their macromolecules to attempt restoration of metabolic homeostasis. Induction of autophagy can result from activation of the unfolded protein response following metabolic stress, the final cell fate often being determined by the extent and duration of autophagy. A study by Gonzalez-Malerva and colleagues builds upon this extensive knowledge, adding HSPB8 to the list of altered genes associated with endocrine resistance in breast cancer and describing the ability of HSPB8 to regulate autophagy and confer tamoxifen resistance.
authors: Department of Oncology, W405A Research Building, Georgetown University Medical Center, 3970 Reservoir Road NW, Washington, DC 20057, USA. clarker@georgetown.edu
authors: Robert
authors: R
authors: Clarke
mesh_terms: D001343:Autophagy / Q000502:physiology*; D001943:Breast Neoplasms / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology*; D002470:Cell Survival; D019008:Drug Resistance, Neoplasm; D047628:Estrogen Receptor alpha / Q000378:metabolism*; D005260:Female; D006360:Heat-Shock Proteins / Q000235:genetics / Q000378:metabolism*; D006801:Humans; D018832:Molecular Chaperones; D017346:Protein Serine-Threonine Kinases / Q000235:genetics / Q000378:metabolism*; D013629:Tamoxifen / Q000494:pharmacology
chemical_list: C506487:ESR1 protein, human; D047628:Estrogen Receptor alpha; C413214:HSPB8 protein, human; D006360:Heat-Shock Proteins; D018832:Molecular Chaperones; D013629:Tamoxifen; D017346:Protein Serine-Threonine Kinases