期刊
CANCER CELL
卷 30, 期 4, 页码 563-577出版社
CELL PRESS
DOI: 10.1016/j.ccell.2016.09.005
关键词
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资金
- Prostate Cancer Foundation (PCF) Challenge award
- NIH [1R01CA179100-01A1]
- Damon Runyon Cancer Research Foundation [CI-67-13]
- Department of Defense [PC121341]
- Early Detection Research Network NCI [U01 CA111275]
- European Research Council [ERCCoG648670, R01 CA116337]
- Translational Research Program at WCM Pathology and Laboratory Medicine
- PhRMA Foundation
- American-Italian Cancer Foundation Post-Doctoral Research Fellowship
- PCF Young Investigator Award
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 off Polycomb Repressive Complex 2 signaling. Altogether, our data establishes N-Myc as an oncogenic driver of NEPC.
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