ATM Is Required for the Prolactin-Induced HSP90-Mediated Increase in Cellular Viability and Clonogenic Growth After DNA Damage.
作者： Ödül Karayazi Atici , Anna Urbanska , Sesha Gopal Gopinathan , Florence Boutillon , Vincent Goffin
关键词:
摘要: Prolactin (PRL) acts as a survival factor for breast cancer cells, but the PRL signaling pathway and mechanism are unknown. Previously, we identified master chaperone, heat shock protein 90 (HSP90) α, prolactin-Janus kinase 2 (JAK2)-signal transducer activator of transcription 5 (STAT5) target gene involved in survival, here investigated role HSP90 PRL-induced viability response to DNA damage. The ataxia-telangiectasia mutated (ATM) plays critical cellular double-strand We observed that increased cells treated with doxorubicin or etoposide. increase resistance is specific receptor, because receptor antagonist, Δ1-9-G129R-hPRL, prevented viability. Two different inhibitors, 17-allylamino-17-demethoxygeldanamycin BIIB021, reduced PRL-mediated cell doxorubicin-treated led decrease JAK2, ATM, phosphorylated ATM levels. Inhibitors JAK2 (G6) (KU55933) abolished DNA-damaged supporting involvement each, well crosstalk context Drug synergism was detected between inhibitor (BIIB021) doxorubicin. Short interfering RNA directed against two-dimensional culture, three-dimensional collagen gel cultures, clonogenic after treatment. Our results indicate contributes PRL-JAK2-STAT5-HSP90 mediating DNA-damaging agents.
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