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N-Myc Induces an EZH2-Mediated Transcriptional Program Driving Neuroendocrine Prostate Cancer. | LitMetric

N-Myc Induces an EZH2-Mediated Transcriptional Program Driving Neuroendocrine Prostate Cancer.

Cancer Cell

Department of Pathology and Laboratory Medicine, Weill Cornell Medicine, New York, NY 10065, USA; Meyer Cancer Center, Weill Cornell Medicine, New York, NY 10065, USA; Englander Institute for Precision Medicine, New York-Presbyterian Hospital, Weill Cornell Medicine, New York, NY 10065, USA. Electronic address:

Published: October 2016

AI Article Synopsis

Article Abstract

The transition from castration-resistant prostate adenocarcinoma (CRPC) to neuroendocrine prostate cancer (NEPC) has emerged as an important mechanism of treatment resistance. NEPC is associated with overexpression and gene amplification of MYCN (encoding N-Myc). N-Myc is an established oncogene in several rare pediatric tumors, but its role in prostate cancer progression is not well established. Integrating a genetically engineered mouse model and human prostate cancer transcriptome data, we show that N-Myc overexpression leads to the development of poorly differentiated, invasive prostate cancer that is molecularly similar to human NEPC. This includes an abrogation of androgen receptor signaling and induction of Polycomb Repressive Complex 2 signaling. Altogether, our data establishes N-Myc as an oncogenic driver of NEPC.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5540451PMC
http://dx.doi.org/10.1016/j.ccell.2016.09.005DOI Listing

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