Journal
CANCER CELL
Volume 29, Issue 4, Pages 536-547Publisher
CELL PRESS
DOI: 10.1016/j.ccell.2016.03.001
Keywords
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Funding
- NIH [U54 HG006097, U54 HL127365, K08NS079485, 5R01CA172603-02, 2P30CA016042-39, 1R01CA181242-01A1, 1R01CA195505, U01 CA164188-01A]
- UCLA Hal Gaba Director's Fund for Cancer Stem Cell Research
- Tower Cancer Research Foundation Career Development Award
- Prostate Cancer Foundation Young Investigator Award
- UCLA Subspecialty Training and Advanced Research Program
- UCLA Tumor Cell Biology Training Grant [T32CA09056]
- UCLA Tumor Immunology Training Grant [T32CA009120]
- UCLA Broad Stem Cell Research Center Training Grant
- Prostate Cancer Foundation
- NCI/NIH [K99CA184397]
- Department of Defense Prostate Cancer Research Program [W81XWH-12-1-0206]
- UCLA SPORE in Prostate Cancer
- Prostate Cancer Foundation Honorable A. David Mazzone Special Challenge Award
- UCLA Jonsson Comprehensive Cancer Center Impact Grant
- Prostate Cancer Foundation Challenge Award
- Stand Up To Cancer/Prostate Cancer Foundation/Prostate Dream Team Translational Cancer Research Grant [SU2C-AACR-DT0812]
- Movember Foundation
- Alex's Lemonade Stand Foundation
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MYCN amplification and overexpression are common in neuroendocrine prostate cancer (NEPC). However, the impact of aberrant N-Myc expression in prostate tumorigenesis and the cellular origin of NEPC have not been established. We define N-Myc and activated AKT1 as oncogenic components sufficient to transform human prostate epithelial cells to prostate adenocarcinoma and NEPC with phenotypic and molecular features of aggressive, late-stage human disease. We directly show that prostate adenocarcinoma and NEPC can arise from a common epithelial clone. Further, N-Myc is required for tumor maintenance, and destabilization of N-Myc through Aurora A kinase inhibition reduces tumor burden. Our findings establish N-Myc as a driver of NEPC and a target for therapeutic intervention.
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