Stat3 regulates centrosome clustering in cancer cells via Stathmin/PLK1

摘要: Cancer cells frequently have amplified centrosomes that must be clustered together to form a bipolar mitotic spindle, and targeting centrosome clustering is considered promising therapeutic strategy. A high-content chemical screen for inhibitors of identified Stattic, Stat3 inhibitor. depletion inhibition in cancer cell lines tumours vivo caused significant viability. Here we describe transcription-independent mechanism Stat3-mediated involves Stathmin, interactor involved microtubule depolymerization, the kinase PLK1. Furthermore, PLK4-driven breast tumour are highly sensitive inhibitors. We an unexpected role regulation clustering, this may critical identifying