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N-Myc Induces an EZH2-Mediated Transcriptional Program Driving Neuroendocrine Prostate Cancer
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Summary 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 over-expression 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 over-expression leads to the development of poorly differentiated, invasive prostate cancer that is molecularly similar to human NEPC. This includes an abrogation of AR 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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Metadata
- Authors
- Dardenne, E., Beltran, H., Benelli, M., Gayvert, K., Berger, A., Puca, L., Cyrta, J., Sboner, A., Noorzad, Z., MacDonald, T., Cheung, C., Yuen, K. S., Gao, D., Chen, Y., Eilers, M., Mosquera, J.-M., Robinson, B. D., Elemento, O., Rubin, M. A., Demichelis, F., & Rickman, D. S.
- Venue
- Cancer Cell
- Publisher
- Elsevier BV
- Published
- 2016-10
- Volume
- 30
- Issue
- 4
- Pages
- 563-577
- ISSN
- 1535-6108 (ISSN-L)
- OpenAlex
- W2530065228
- Cited by
- 559
- References
- 45
- FWCI
- 34.69
- Type
- journal article
- Language
- en
- Open access
- bronze
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