بيانات النشر: Uppsala universitet, Neuroonkologi
Uppsala universitet, Institutionen för immunologi, genetik och patologi
Karolinska Inst, Dept Physiol & Pharmacol, S-17177 Stockholm, Sweden
Weill Cornell Med, Dept Physiol & Biophys, New York, NY 10065 USA
Weill Cornell Med, Meyer Canc Ctr, New York, NY 10065 USA;Weill Cornell Med Coll, Dept Pediat & Cell & Dev Biol, New York, NY 10065 USA
Karolinska Inst, Dept Physiol & Pharmacol, S-17177 Stockholm, Sweden;Med Univ Vienna, Dept Brain Res, A-1090 Vienna, Austria
Stockholm Univ, Dept Mol Biosci, Wenner Gren Inst, S-10691 Stockholm, Sweden
Weill Cornell Med, Dept Physiol & Biophys, New York, NY 10065 USA;Weill Cornell Med, Meyer Canc Ctr, New York, NY 10065 USA
Lund Univ, Dept Lab Med, Ctr Mol Pathol, SE-22381 Lund, Sweden
Karolinska Inst, Dept Cell & Mol Biol, SE-17177 Stockholm, Sweden
Albert Einstein Coll Med, Gruss Lipper Biophoton Ctr, Bronx, NY 10461 USA;Montefiore Med Ctr, Dept Pathol, Bronx, NY 10461 USA
Rockefeller Univ, Lab Chromatin Biol & Epigenet, New York, NY 10065 USA
Pimera Inc, 3210 Merryfield Row, San Diego, CA 92121 USA
UMH, CSIC, Inst Neurociencias, Alicante 03550, Spain
New York Univ Abu Dhabi, Div Sci, Biol Program, Abu Dhabi 129188, U Arab Emirates
Karolinska Inst, Dept Pathol & Oncol, S-17176 Solna, Sweden;Univ Hosp, S-17176 Solna, Sweden
Weill Cornell Med, Dept Physiol & Biophys, New York, NY 10065 USA;Weill Cornell Med, Meyer Canc Ctr, New York, NY 10065 USA;Weill Cornell Med, Triinst Training Program Chem Biol, New York, NY 10065 USA
Karolinska Inst, Dept Physiol & Pharmacol, S-17177 Stockholm, Sweden;Weill Cornell Med, Dept Physiol & Biophys, New York, NY 10065 USA;Weill Cornell Med, Meyer Canc Ctr, New York, NY 10065 USA
نبذة مختصرة : 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. ; De 2 första författarna delar förstaförfattarskapet.
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