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Ribosome biogenesis during cell cycle arrest fuels EMT in development and disease
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Number of Authors: 282019 (English)In: Nature Communications, ISSN 2041-1723, E-ISSN 2041-1723, Vol. 10, article id 2110Article in journal (Refereed) Published
Abstract [en]

Ribosome biogenesis is a canonical hallmark of cell growth and proliferation. Here we show that execution of Epithelial-to-Mesenchymal Transition (EMT), a migratory cellular program associated with development and tumor metastasis, is fueled by upregulation of ribosome biogenesis during G1/S arrest. This unexpected EMT feature is independent of species and initiating signal, and is accompanied by release of the repressive nucleolar chromatin remodeling complex (NoRC) from rDNA, together with recruitment of the EMT-driving transcription factor Snai1 (Snail1), RNA Polymerase I (Pol I) and the Upstream Binding Factor (UBF). EMT-associated ribosome biogenesis is also coincident with increased nucleolar recruitment of Rictor, an essential component of the EMT-promoting mammalian target of rapamycin complex 2 (mTORC2). Inhibition of rRNA synthesis in vivo differentiates primary tumors to a benign, Estrogen Receptor-alpha (ER alpha) positive, Rictor-negative phenotype and reduces metastasis. These findings implicate the EMT-associated ribosome biogenesis program with cellular plasticity, de-differentiation, cancer progression and metastatic disease.

Place, publisher, year, edition, pages
2019. Vol. 10, article id 2110
National Category
Biological Sciences
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URN: urn:nbn:se:su:diva-169248DOI: 10.1038/s41467-019-10100-8ISI: 000467371400008PubMedID: 31068593OAI: oai:DiVA.org:su-169248DiVA, id: diva2:1323736
Available from: 2019-06-12 Created: 2019-06-12 Last updated: 2019-06-12Bibliographically approved

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Petersen, JulianGuo, YuanÖstlund Farrants, Ann-Kristin
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Department of Molecular Biosciences, The Wenner-Gren Institute
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