Pan-cancer genetic analysis identifies PARK2 as a master regulator of G1/S cyclins View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2014-06

AUTHORS

Yongxing Gong, Travis Ian Zack, Luc G T Morris, Kan Lin, Ellen Hukkelhoven, Radhika Raheja, I-Li Tan, Sevin Turcan, Selvaraju Veeriah, Shasha Meng, Agnes Viale, Steven E Schumacher, Perry Palmedo, Rameen Beroukhim, Timothy A Chan

ABSTRACT

Coordinate control of different classes of cyclins is fundamentally important for cell cycle regulation and tumor suppression, yet the underlying mechanisms are incompletely understood. Here we show that the PARK2 tumor suppressor mediates this coordination. The PARK2 E3 ubiquitin ligase coordinately controls the stability of both cyclin D and cyclin E. Analysis of approximately 5,000 tumor genomes shows that PARK2 is a very frequently deleted gene in human cancer and uncovers a striking pattern of mutual exclusivity between PARK2 deletion and amplification of CCND1, CCNE1 or CDK4-implicating these genes in a common pathway. Inactivation of PARK2 results in the accumulation of cyclin D and acceleration of cell cycle progression. Furthermore, PARK2 is a component of a new class of cullin-RING-containing ubiquitin ligases targeting both cyclin D and cyclin E for degradation. Thus, PARK2 regulates cyclin-CDK complexes, as does the CDK inhibitor p16, but acts as a master regulator of the stability of G1/S cyclins. More... »

PAGES

588-594

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  • Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1038/ng.2981

    DOI

    http://dx.doi.org/10.1038/ng.2981

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1013606458

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/24793136


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