Suppression of KRas-mutant cancer through the combined inhibition of KRAS with PLK1 and ROCK

KRas is frequently mutated in multiple cancer types; identifying drugs to treat such cancers is a good therapeutic strategy. Here, the authors perform a synthetic lethal screen in mice and show that inhibiting Plk1 and ROCK results in the inhibition of tumour growth by increasing expression of the t...

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Main Authors:	Jieqiong Wang, Kewen Hu, Jiawei Guo, Feixiong Cheng, Jing Lv, Wenhao Jiang, Weiqiang Lu, Jinsong Liu, Xiufeng Pang, Mingyao Liu
Format:	Article
Language:	English
Published:	Nature Publishing Group 2016-05-01
Series:	Nature Communications
Online Access:	https://doi.org/10.1038/ncomms11363

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spelling	doaj-0c74c6b0573c4f9f816fe66db2394a142021-05-11T11:10:50ZengNature Publishing GroupNature Communications2041-17232016-05-017111310.1038/ncomms11363Suppression of KRas-mutant cancer through the combined inhibition of KRAS with PLK1 and ROCKJieqiong Wang0Kewen Hu1Jiawei Guo2Feixiong Cheng3Jing Lv4Wenhao Jiang5Weiqiang Lu6Jinsong Liu7Xiufeng Pang8Mingyao Liu9Shanghai Key Laboratory of Regulatory Biology, Institute of Biomedical Sciences and School of Life Sciences, East China Normal UniversityShanghai Key Laboratory of Regulatory Biology, Institute of Biomedical Sciences and School of Life Sciences, East China Normal UniversityShanghai Key Laboratory of Regulatory Biology, Institute of Biomedical Sciences and School of Life Sciences, East China Normal UniversityState Key Laboratory of Biotherapy/Collaborative Innovation Center for Biotherapy, West China Hospital, West China Medical School, Sichuan UniversityShanghai Key Laboratory of Regulatory Biology, Institute of Biomedical Sciences and School of Life Sciences, East China Normal UniversityShanghai Key Laboratory of Regulatory Biology, Institute of Biomedical Sciences and School of Life Sciences, East China Normal UniversityShanghai Key Laboratory of Regulatory Biology, Institute of Biomedical Sciences and School of Life Sciences, East China Normal UniversityDepartment of Pathology, The University of Texas MD Anderson Cancer CenterShanghai Key Laboratory of Regulatory Biology, Institute of Biomedical Sciences and School of Life Sciences, East China Normal UniversityShanghai Key Laboratory of Regulatory Biology, Institute of Biomedical Sciences and School of Life Sciences, East China Normal UniversityKRas is frequently mutated in multiple cancer types; identifying drugs to treat such cancers is a good therapeutic strategy. Here, the authors perform a synthetic lethal screen in mice and show that inhibiting Plk1 and ROCK results in the inhibition of tumour growth by increasing expression of the tumour suppressor p21.https://doi.org/10.1038/ncomms11363
collection	DOAJ
language	English
format	Article
sources	DOAJ
author	Jieqiong Wang Kewen Hu Jiawei Guo Feixiong Cheng Jing Lv Wenhao Jiang Weiqiang Lu Jinsong Liu Xiufeng Pang Mingyao Liu
spellingShingle	Jieqiong Wang Kewen Hu Jiawei Guo Feixiong Cheng Jing Lv Wenhao Jiang Weiqiang Lu Jinsong Liu Xiufeng Pang Mingyao Liu Suppression of KRas-mutant cancer through the combined inhibition of KRAS with PLK1 and ROCK Nature Communications
author_facet	Jieqiong Wang Kewen Hu Jiawei Guo Feixiong Cheng Jing Lv Wenhao Jiang Weiqiang Lu Jinsong Liu Xiufeng Pang Mingyao Liu
author_sort	Jieqiong Wang
title	Suppression of KRas-mutant cancer through the combined inhibition of KRAS with PLK1 and ROCK
title_short	Suppression of KRas-mutant cancer through the combined inhibition of KRAS with PLK1 and ROCK
title_full	Suppression of KRas-mutant cancer through the combined inhibition of KRAS with PLK1 and ROCK
title_fullStr	Suppression of KRas-mutant cancer through the combined inhibition of KRAS with PLK1 and ROCK
title_full_unstemmed	Suppression of KRas-mutant cancer through the combined inhibition of KRAS with PLK1 and ROCK
title_sort	suppression of kras-mutant cancer through the combined inhibition of kras with plk1 and rock
publisher	Nature Publishing Group
series	Nature Communications
issn	2041-1723
publishDate	2016-05-01
description	KRas is frequently mutated in multiple cancer types; identifying drugs to treat such cancers is a good therapeutic strategy. Here, the authors perform a synthetic lethal screen in mice and show that inhibiting Plk1 and ROCK results in the inhibition of tumour growth by increasing expression of the tumour suppressor p21.
url	https://doi.org/10.1038/ncomms11363
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Suppression of KRas-mutant cancer through the combined inhibition of KRAS with PLK1 and ROCK

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