Regulation of survivin function by Hsp90

摘要: Pathways controlling cell proliferation and survival require flexible adaptation to environmental stresses. These mechanisms are frequently exploited in cancer, allowing tumor cells thrive unfavorable milieus. Here, we show that Hsp90, a molecular chaperone is central the cellular stress response, associates with survivin, an apoptosis inhibitor essential regulator of mitosis. This interaction involves ATPase domain Hsp90 survivin baculovirus repeat. Global suppression function or targeted Abmediated disruption survivin–Hsp90 complex results proteasomal degradation mitochondrial-dependent apoptosis, cycle arrest mitotic defects. data link response antiapoptotic checkpoint maintained by survivin. Targeting may provide rational approach for cancer therapy.