Journal article
The p53 isoform Δ133p53β promotes cancer stem cell potential
N Arsic, G Gadea, EL Lagerqvist, M Bußon, N Cahuzac, C Brock, F Hollande, V Gire, J Pannequin, P Roux
Stem Cell Reports | CELL PRESS | Published : 2015
Abstract
Cancer stem cells (CSC) are responsible for cancer chemoresistance and metastasis formation. Here we report that Δ133p53β, a TP53 splice variant, enhanced cancer cell stemneß in MCF-7 breast cancer cells, while its depletion reduced it. Δ133p53β stimulated the expreßion of the key pluripotency factors SOX2, OCT3/4, and NANOG. Similarly, in highly metastatic breast cancer cells, aggreßiveneß was coupled with enhanced CSC potential and Δ133p53β expreßion. Like in MCF-7 cells, SOX2, OCT3/4, and NANOG expreßion were positively regulated by Δ133p53β in these cells. Finally, treatment of MCF-7 cells with etoposide, a cytotoxic anti-cancer drug, increased CSC formation and SOX2, OCT3/4, and NANOG e..
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Funding Acknowledgements
We are grateful to Montpellier Rio Imaging (MRI) for constructive microscopy; P. Fort and E. Andermacher for critical comments on the manuscript; C. Vincent, Y. Buscail, and N. Pirot for in vivo experiments (Animal facility and RHEM facility [Reseau d'histologie experimentale de Montpellier], respectively); and J.-C. Bourdon (University of Dundee, UK) for plasmids and helpful discussion. G.G., N.A., and P.R. are supported by Centre National de la Recherche Scientifique (CNRS) and Institut National de la Sante et de la Recherche Medicale (INSERM).