Oncogenic KRAS supports pancreatic cancer through regulation of nucleotide synthesis

Pancreatic ductal adenocarcinoma (PDAC) cells display varying degrees of reliance on oncogenic KRAS. Here the authors show that KRAS-resistant PDAC cells maintain nucleotides synthesis through a KRAS-independent upregulation of the non-oxidative pentose phosphate pathway gene RPIA and that targeting...

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Autores principales: Naiara Santana-Codina, Anjali A. Roeth, Yi Zhang, Annan Yang, Oksana Mashadova, John M. Asara, Xiaoxu Wang, Roderick T. Bronson, Costas A. Lyssiotis, Haoqiang Ying, Alec C. Kimmelman
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Lenguaje:EN
Publicado: Nature Portfolio 2018
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Acceso en línea:https://doaj.org/article/54e4abc4188c4609baed834f3f363f66
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spelling oai:doaj.org-article:54e4abc4188c4609baed834f3f363f662021-12-02T16:50:12ZOncogenic KRAS supports pancreatic cancer through regulation of nucleotide synthesis10.1038/s41467-018-07472-82041-1723https://doaj.org/article/54e4abc4188c4609baed834f3f363f662018-11-01T00:00:00Zhttps://doi.org/10.1038/s41467-018-07472-8https://doaj.org/toc/2041-1723Pancreatic ductal adenocarcinoma (PDAC) cells display varying degrees of reliance on oncogenic KRAS. Here the authors show that KRAS-resistant PDAC cells maintain nucleotides synthesis through a KRAS-independent upregulation of the non-oxidative pentose phosphate pathway gene RPIA and that targeting nucleotide metabolism restore sensitivity to KRAS pathway inhibition.Naiara Santana-CodinaAnjali A. RoethYi ZhangAnnan YangOksana MashadovaJohn M. AsaraXiaoxu WangRoderick T. BronsonCostas A. LyssiotisHaoqiang YingAlec C. KimmelmanNature PortfolioarticleScienceQENNature Communications, Vol 9, Iss 1, Pp 1-13 (2018)
institution DOAJ
collection DOAJ
language EN
topic Science
Q
spellingShingle Science
Q
Naiara Santana-Codina
Anjali A. Roeth
Yi Zhang
Annan Yang
Oksana Mashadova
John M. Asara
Xiaoxu Wang
Roderick T. Bronson
Costas A. Lyssiotis
Haoqiang Ying
Alec C. Kimmelman
Oncogenic KRAS supports pancreatic cancer through regulation of nucleotide synthesis
description Pancreatic ductal adenocarcinoma (PDAC) cells display varying degrees of reliance on oncogenic KRAS. Here the authors show that KRAS-resistant PDAC cells maintain nucleotides synthesis through a KRAS-independent upregulation of the non-oxidative pentose phosphate pathway gene RPIA and that targeting nucleotide metabolism restore sensitivity to KRAS pathway inhibition.
format article
author Naiara Santana-Codina
Anjali A. Roeth
Yi Zhang
Annan Yang
Oksana Mashadova
John M. Asara
Xiaoxu Wang
Roderick T. Bronson
Costas A. Lyssiotis
Haoqiang Ying
Alec C. Kimmelman
author_facet Naiara Santana-Codina
Anjali A. Roeth
Yi Zhang
Annan Yang
Oksana Mashadova
John M. Asara
Xiaoxu Wang
Roderick T. Bronson
Costas A. Lyssiotis
Haoqiang Ying
Alec C. Kimmelman
author_sort Naiara Santana-Codina
title Oncogenic KRAS supports pancreatic cancer through regulation of nucleotide synthesis
title_short Oncogenic KRAS supports pancreatic cancer through regulation of nucleotide synthesis
title_full Oncogenic KRAS supports pancreatic cancer through regulation of nucleotide synthesis
title_fullStr Oncogenic KRAS supports pancreatic cancer through regulation of nucleotide synthesis
title_full_unstemmed Oncogenic KRAS supports pancreatic cancer through regulation of nucleotide synthesis
title_sort oncogenic kras supports pancreatic cancer through regulation of nucleotide synthesis
publisher Nature Portfolio
publishDate 2018
url https://doaj.org/article/54e4abc4188c4609baed834f3f363f66
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AT anjaliaroeth oncogenickrassupportspancreaticcancerthroughregulationofnucleotidesynthesis
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