Stat3 regulates centrosome clustering in cancer cells via Stathmin/PLK1

Edward J. Morris (), Eiko Kawamura, Jordan A. Gillespie, Aruna Balgi, Nagarajan Kannan, William J. Muller, Michel Roberge and Shoukat Dedhar ()
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Edward J. Morris: BC Cancer Research Centre, BC Cancer Agency
Eiko Kawamura: BC Cancer Research Centre, BC Cancer Agency
Jordan A. Gillespie: BC Cancer Research Centre, BC Cancer Agency
Aruna Balgi: Life Sciences Institute, University of British Columbia
Nagarajan Kannan: Terry Fox Laboratory, BC Cancer Agency
William J. Muller: Rosalind and Morris Goodman Cancer Centre, McGill University
Michel Roberge: Life Sciences Institute, University of British Columbia
Shoukat Dedhar: BC Cancer Research Centre, BC Cancer Agency

Nature Communications, 2017, vol. 8, issue 1, 1-15

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

Date: 2017
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DOI: 10.1038/ncomms15289

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