Targeting KRAS4A splicing through the RBM39/DCAF15 pathway inhibits cancer stem cells

Kras is frequently mutated in lung cancer and two isoforms are generated via alternative splicing. Here, the authors show that the two isoforms have divergent roles in cancer stem cells and the main tumour cell population, which are regulated by hypoxia and endoplasmic reticulum stress.

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Autores principales:	Wei-Ching Chen, Minh D. To, Peter M. K. Westcott, Reyno Delrosario, Il-Jin Kim, Mark Philips, Quan Tran, Saumya R. Bollam, Hani Goodarzi, Nora Bayani, Olga Mirzoeva, Allan Balmain
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2021
Materias:	Science Q
Acceso en línea:	https://doaj.org/article/a22b5d5de40945018011a5128be0357a
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spelling	oai:doaj.org-article:a22b5d5de40945018011a5128be0357a2021-12-02T15:33:16ZTargeting KRAS4A splicing through the RBM39/DCAF15 pathway inhibits cancer stem cells10.1038/s41467-021-24498-72041-1723https://doaj.org/article/a22b5d5de40945018011a5128be0357a2021-07-01T00:00:00Zhttps://doi.org/10.1038/s41467-021-24498-7https://doaj.org/toc/2041-1723Kras is frequently mutated in lung cancer and two isoforms are generated via alternative splicing. Here, the authors show that the two isoforms have divergent roles in cancer stem cells and the main tumour cell population, which are regulated by hypoxia and endoplasmic reticulum stress.Wei-Ching ChenMinh D. ToPeter M. K. WestcottReyno DelrosarioIl-Jin KimMark PhilipsQuan TranSaumya R. BollamHani GoodarziNora BayaniOlga MirzoevaAllan BalmainNature PortfolioarticleScienceQENNature Communications, Vol 12, Iss 1, Pp 1-14 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Science Q
spellingShingle	Science Q Wei-Ching Chen Minh D. To Peter M. K. Westcott Reyno Delrosario Il-Jin Kim Mark Philips Quan Tran Saumya R. Bollam Hani Goodarzi Nora Bayani Olga Mirzoeva Allan Balmain Targeting KRAS4A splicing through the RBM39/DCAF15 pathway inhibits cancer stem cells
description	Kras is frequently mutated in lung cancer and two isoforms are generated via alternative splicing. Here, the authors show that the two isoforms have divergent roles in cancer stem cells and the main tumour cell population, which are regulated by hypoxia and endoplasmic reticulum stress.
format	article
author	Wei-Ching Chen Minh D. To Peter M. K. Westcott Reyno Delrosario Il-Jin Kim Mark Philips Quan Tran Saumya R. Bollam Hani Goodarzi Nora Bayani Olga Mirzoeva Allan Balmain
author_facet	Wei-Ching Chen Minh D. To Peter M. K. Westcott Reyno Delrosario Il-Jin Kim Mark Philips Quan Tran Saumya R. Bollam Hani Goodarzi Nora Bayani Olga Mirzoeva Allan Balmain
author_sort	Wei-Ching Chen
title	Targeting KRAS4A splicing through the RBM39/DCAF15 pathway inhibits cancer stem cells
title_short	Targeting KRAS4A splicing through the RBM39/DCAF15 pathway inhibits cancer stem cells
title_full	Targeting KRAS4A splicing through the RBM39/DCAF15 pathway inhibits cancer stem cells
title_fullStr	Targeting KRAS4A splicing through the RBM39/DCAF15 pathway inhibits cancer stem cells
title_full_unstemmed	Targeting KRAS4A splicing through the RBM39/DCAF15 pathway inhibits cancer stem cells
title_sort	targeting kras4a splicing through the rbm39/dcaf15 pathway inhibits cancer stem cells
publisher	Nature Portfolio
publishDate	2021
url	https://doaj.org/article/a22b5d5de40945018011a5128be0357a
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Targeting KRAS4A splicing through the RBM39/DCAF15 pathway inhibits cancer stem cells

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