Genome-wide CRISPR-Cas9 Screens Reveal Loss of Redundancy between PKMYT1 and WEE1 in Glioblastoma Stem-like Cells
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- 作者：Chad M. Toledo1 ; 2 ; 14 ; Yu Ding1 ; 14 ; Pia Hoellerbauer1 ; 2 ; Ryan J. Davis1 ; 2 ; 3 ; Ryan Basom4 ; Emily J. Girard3 ; Eunjee Lee5 ; Philip Corrin1 ; Traver Hart6 ; 7 ; Hamid Bolouri1 ; Jerry Davison4 ; Qing Zhang4 ; Justin Hardcastle1 ; Bruce J. Aronow8 ; Christopher L. Plaisier9 ; Nitin S. Baliga9 ; Jason Moffat6 ; 7 ; Qi Lin10 ; Xiao-Nan Li10 ; Do-Hyun Nam11 ; Jeongwu Lee12 ; Steven M. Pollard13 ; Jun Zhu5 ; Jeffery J. Delrow4 ; Bruce E. Clurman1 ; 3 ; James M. Olson3 ; jolson@fredhutch.org" class="auth_mail" title="E-mail the corresponding author ; Patrick J. Paddison1 ; 2 ; paddison@fredhutch.org" class="auth_mail" title="E-mail the corresponding author
- 关键词：CRISPR-Cas9 ; gene editing ; Glioblastoma ; PKMYT1 ; Myt1 ; WEE1 ; cancer therapeutics ; functional genomics
- 刊名：Cell Reports
- 出版年：2015
- 出版时间：22 December 2015
- 年：2015
- 卷：13
- 期：11
- 页码：2425-2439
- 全文大小：3415 K
文摘
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CRISPR-Cas9 lethality screens performed in patient brain-tumor stem-like cells
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PKMYT1 is identified in GSCs, but not NSCs, as essential for facilitating mitosis
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PKMYT1 and WEE1 act redundantly in NSCs, where their inhibition is synthetic lethal
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PKMYT1 and WEE1 redundancy can be broken by over-activation of EGFR and AKT