Unconventional role of RAC1 in MET-driven anchorage-independent tumor growth

We reported that RAC1 is a master regulator of cell migration and anchorage-independent growth, downstream of the oncogenic Receptor Tyrosine Kinase (RTK) MET. RAC1 growth-promoting role is guanosine triphosphatase (GTPase)- and phosphatidylinositol 3-kinase (PI3K)-independent but promotes mammalian...

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Detalles Bibliográficos
Autores principales: Hervieu, Alexia, Kermorgant, Stéphanie
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Taylor & Francis 2020
Materias:
Author’s Views
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7671004/
https://www.ncbi.nlm.nih.gov/pubmed/33235904
http://dx.doi.org/10.1080/23723556.2020.1803029
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author Hervieu, Alexia
Kermorgant, Stéphanie
author_facet Hervieu, Alexia
Kermorgant, Stéphanie
author_sort Hervieu, Alexia
collection PubMed
description We reported that RAC1 is a master regulator of cell migration and anchorage-independent growth, downstream of the oncogenic Receptor Tyrosine Kinase (RTK) MET. RAC1 growth-promoting role is guanosine triphosphatase (GTPase)- and phosphatidylinositol 3-kinase (PI3K)-independent but promotes mammalian target of rapamycin (mTOR) signaling through triggering its plasma membrane localization.
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spelling pubmed-76710042020-11-23 Unconventional role of RAC1 in MET-driven anchorage-independent tumor growth Hervieu, Alexia Kermorgant, Stéphanie Mol Cell Oncol Author’s Views We reported that RAC1 is a master regulator of cell migration and anchorage-independent growth, downstream of the oncogenic Receptor Tyrosine Kinase (RTK) MET. RAC1 growth-promoting role is guanosine triphosphatase (GTPase)- and phosphatidylinositol 3-kinase (PI3K)-independent but promotes mammalian target of rapamycin (mTOR) signaling through triggering its plasma membrane localization. Taylor & Francis 2020-08-18 /pmc/articles/PMC7671004/ /pubmed/33235904 http://dx.doi.org/10.1080/23723556.2020.1803029 Text en © 2020 The Author(s). Published with license by Taylor & Francis Group, LLC. https://creativecommons.org/licenses/by-nc-nd/4.0/This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivatives License (http://creativecommons.org/licenses/by-nc-nd/4.0/ (https://creativecommons.org/licenses/by-nc-nd/4.0/) ), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited, and is not altered, transformed, or built upon in any way.
spellingShingle Author’s Views
Hervieu, Alexia
Kermorgant, Stéphanie
Unconventional role of RAC1 in MET-driven anchorage-independent tumor growth
title Unconventional role of RAC1 in MET-driven anchorage-independent tumor growth
title_full Unconventional role of RAC1 in MET-driven anchorage-independent tumor growth
title_fullStr Unconventional role of RAC1 in MET-driven anchorage-independent tumor growth
title_full_unstemmed Unconventional role of RAC1 in MET-driven anchorage-independent tumor growth
title_short Unconventional role of RAC1 in MET-driven anchorage-independent tumor growth
title_sort unconventional role of rac1 in met-driven anchorage-independent tumor growth
topic Author’s Views
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7671004/
https://www.ncbi.nlm.nih.gov/pubmed/33235904
http://dx.doi.org/10.1080/23723556.2020.1803029
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