BCL9L Dysfunction Impairs Caspase-2 Expression Permitting Aneuploidy Tolerance in Colorectal Cancer

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• 作者：Carlos L&oacute ; pez-Garc&iacute ; a¹ ; Laurent Sansregret¹ ; Enric Domingo⁵ ; ⁶ ; Nicholas McGranahan¹ ; ⁷ ; Sebastijan Hobor¹ ; Nicolai Juul Birkbak¹ ; ⁷ ; Stuart Horswell² ; Eva Grö ; nroos¹ ; Francesco Favero¹ ; ⁸ ; Andrew J. Rowan¹ ; Nicholas Matthews⁴ ; Sharmin Begum⁴ ; Benjamin Phillimore⁴ ; Rebecca Burrell¹ ; Dahmane Oukrif⁹ ; Bradley Spencer-Dene³ ; Michal Kovac⁵ ; Gordon Stamp³ ; Aengus Stewart² ; Havard Danielsen¹⁰ ; Marco Novelli⁹ ; Ian Tomlinson⁵ ; Charles Swanton¹ ; ⁷ ; ¹¹ ; ^{charles.swanton@crick.ac.uk}
• 关键词：aneuploidy tolerance ; chromosomal instability ; BCL9L ; caspase-2 ; p53 ; intratumor heterogeneity ; chromosome segregation errors ; mitotic checkpoint ; BID ; colorectal cancer evolution
• 刊名：Cancer Cell
• 出版年：2017
• 出版时间：9 January 2017
• 年：2017
• 卷：31
• 期：1
• 页码：79-93
• 全文大小：2665 K
• 卷排序：31

文摘

Loss-of-function alterations in BCL9L are frequent in aneuploid CRC BCL9L dysfunction drives aneuploidy tolerance by reducing levels of caspase-2 Caspase-2 activation following aneuploidy results in MDM2 and BID cleavage p53 stabilization after chromosome missegregation is regulated by caspase-2