GSK3 suppression upregulates β-catenin and c-Myc to abrogate KRas-dependent tumors

Direct targeting of mutant KRas is challenging and alternative approaches are needed. Here they show glycogen synthase kinase 3 (GSK3) to be required for the growth and survival of human mutant KRas-dependent tumors but dispensable for mutant KRas-independent tumors and show GSK3 inhibition to inhib...

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Autores principales:	Aslamuzzaman Kazi, Shengyan Xiang, Hua Yang, Daniel Delitto, José Trevino, Rays H. Y. Jiang, Muhammad Ayaz, Harshani R. Lawrence, Perry Kennedy, Saïd M. Sebti
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2018
Materias:	Science Q
Acceso en línea:	https://doaj.org/article/e4dd4e549d124d48b1ca42f85db738ff
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spelling	oai:doaj.org-article:e4dd4e549d124d48b1ca42f85db738ff2021-12-02T16:49:22ZGSK3 suppression upregulates β-catenin and c-Myc to abrogate KRas-dependent tumors10.1038/s41467-018-07644-62041-1723https://doaj.org/article/e4dd4e549d124d48b1ca42f85db738ff2018-12-01T00:00:00Zhttps://doi.org/10.1038/s41467-018-07644-6https://doaj.org/toc/2041-1723Direct targeting of mutant KRas is challenging and alternative approaches are needed. Here they show glycogen synthase kinase 3 (GSK3) to be required for the growth and survival of human mutant KRas-dependent tumors but dispensable for mutant KRas-independent tumors and show GSK3 inhibition to inhibit in vivo growth of Kras mutant patient-derived pancreatic tumors.Aslamuzzaman KaziShengyan XiangHua YangDaniel DelittoJosé TrevinoRays H. Y. JiangMuhammad AyazHarshani R. LawrencePerry KennedySaïd M. SebtiNature PortfolioarticleScienceQENNature Communications, Vol 9, Iss 1, Pp 1-9 (2018)
institution	DOAJ
collection	DOAJ
language	EN
topic	Science Q
spellingShingle	Science Q Aslamuzzaman Kazi Shengyan Xiang Hua Yang Daniel Delitto José Trevino Rays H. Y. Jiang Muhammad Ayaz Harshani R. Lawrence Perry Kennedy Saïd M. Sebti GSK3 suppression upregulates β-catenin and c-Myc to abrogate KRas-dependent tumors
description	Direct targeting of mutant KRas is challenging and alternative approaches are needed. Here they show glycogen synthase kinase 3 (GSK3) to be required for the growth and survival of human mutant KRas-dependent tumors but dispensable for mutant KRas-independent tumors and show GSK3 inhibition to inhibit in vivo growth of Kras mutant patient-derived pancreatic tumors.
format	article
author	Aslamuzzaman Kazi Shengyan Xiang Hua Yang Daniel Delitto José Trevino Rays H. Y. Jiang Muhammad Ayaz Harshani R. Lawrence Perry Kennedy Saïd M. Sebti
author_facet	Aslamuzzaman Kazi Shengyan Xiang Hua Yang Daniel Delitto José Trevino Rays H. Y. Jiang Muhammad Ayaz Harshani R. Lawrence Perry Kennedy Saïd M. Sebti
author_sort	Aslamuzzaman Kazi
title	GSK3 suppression upregulates β-catenin and c-Myc to abrogate KRas-dependent tumors
title_short	GSK3 suppression upregulates β-catenin and c-Myc to abrogate KRas-dependent tumors
title_full	GSK3 suppression upregulates β-catenin and c-Myc to abrogate KRas-dependent tumors
title_fullStr	GSK3 suppression upregulates β-catenin and c-Myc to abrogate KRas-dependent tumors
title_full_unstemmed	GSK3 suppression upregulates β-catenin and c-Myc to abrogate KRas-dependent tumors
title_sort	gsk3 suppression upregulates β-catenin and c-myc to abrogate kras-dependent tumors
publisher	Nature Portfolio
publishDate	2018
url	https://doaj.org/article/e4dd4e549d124d48b1ca42f85db738ff
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GSK3 suppression upregulates β-catenin and c-Myc to abrogate KRas-dependent tumors

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