Heat Shock Protein-27 (Hsp-27) in Breast Cancers: Regulation of Expression and Function

摘要: The small heat shock protein, Hsp27, is elevated in a significant proportion of breast cancers. Over-expression Hsp27 cancer cells increases anchorage-independent growth, invasiveness and resistance to chemotherapeutic drugs associated with poor prognosis shorter disease free survival patients. acts complex manner elicit diverse effects e.g. increasing response many stresses by acting either as molecular chaperone, association components the apoptotic machinery and/or cellular glutathione regulate redox state cells. also regulates cytoskeleton organization stability. Therefore, factors that increase expression alter functions can affect progression outcome following treatment. Although be mediated via classical Heat Shock stress, its elevation independent positive regulators which include estrogen receptor (ER) transcription such Brn-3b Sp1. HET/SAF-B negatively these are regulated post-translationally phosphorylation at specific residues, oligomerization protein thus expression, mechanisms described this chapter