Heat-shock protein 70 binds to a novel sequence in 5′ UTR of tumor suppressor SMAR1 and regulates its mRNA stability upon Prostaglandin A2 treatment

AbstractHere, we report Prostaglandin A2 (PGA2) induced binding of HSP70 to a novel site on φ1 SMAR1 5′ UTR which stabilizes the wild type transcript and leads to subsequent increase in SMAR1 protein levels. SMAR1 mediated cell cycle arrest is perturbed in PGA2-treated cells when HSP70 is knocked-down. Contrarily HSP70, unlike SMAR1, is overexpressed in breast cancers. We demonstrate that this is because of the inability of HSP70 to bind to the φ17 SMAR1 UTR variant which is the predominant form in breast cancers