| Literature DB >> 29990501 |
Hanlin Zeng1, Aparna Jorapur1, A Hunter Shain2, Ursula E Lang2, Rodrigo Torres1, Yuntian Zhang1, Andrew S McNeal1, Thomas Botton2, Jue Lin3, Matthew Donne4, Ingmar N Bastian2, Richard Yu5, Jeffrey P North6, Laura Pincus6, Beth S Ruben7, Nancy M Joseph8, Iwei Yeh2, Boris C Bastian2, Robert L Judson9.
Abstract
Loss of the CDKN2A tumor suppressor is associated with melanoma metastasis, but the mechanisms connecting the phenomena are unknown. Using CRISPR-Cas9 to engineer a cellular model of melanoma initiation from primary human melanocytes, we discovered that a lineage-restricted transcription factor, BRN2, is downstream of CDKN2A and directly regulated by E2F1. In a cohort of melanocytic tumors that capture distinct progression stages, we observed that CDKN2A loss coincides with both the onset of invasive behavior and increased BRN2 expression. Loss of the CDKN2A protein product p16INK4A permitted metastatic dissemination of human melanoma lines in mice, a phenotype rescued by inhibition of BRN2. These results demonstrate a mechanism by which CDKN2A suppresses the initiation of melanoma invasion through inhibition of BRN2.Entities:
Keywords: BRN2; CDKN2A; CRISPR engineering; E2F1; invasion; melanocytes; melanoma
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Year: 2018 PMID: 29990501 PMCID: PMC6084788 DOI: 10.1016/j.ccell.2018.05.014
Source DB: PubMed Journal: Cancer Cell ISSN: 1535-6108 Impact factor: 31.743