4.8 Article

NSD2 is a conserved driver of metastatic prostate cancer progression

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NATURE COMMUNICATIONS
卷 9, 期 -, 页码 -

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NATURE PORTFOLIO
DOI: 10.1038/s41467-018-07511-4

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资金

  1. Flow Cytometry Core
  2. JP Sulzberger Columbia Genome Center
  3. Small Animal Imaging Facility
  4. NIH/NCI [P30 CA013696]
  5. National Cancer Institute [CA173481, CA196662, U54 CA209997, P50 CA211024, R35 CA197745]
  6. TJ Martell Foundation for Leukemia, Cancer and AIDS Research
  7. Instituto de Salut Carlos III [PI16/01070, CP15/00090]
  8. European Association of Urology Research Foundation [EAURF/407003/XH]
  9. Fundacion BBVA
  10. CERCA Program/Generalitat de Catalunya
  11. FEDER funds/European Regional Development Fund (ERDF)-a way to Build Europe
  12. DOD Prostate Cancer Research Program [PC150959, PC141549]
  13. International Cancer Research Fellowship Outgoing - Associazione Italiana per la Ricerca sul Cancro (AIRC)
  14. Marie Curie Actions COFUND
  15. Department of Defense Award [W81XWH-18-1-0193]
  16. Nuovo-Soldati Foundation
  17. Irving Institute/Clinical Trials Office (CTO) Pilot Award [UR002765-01]
  18. Irving Institute for Clinical and Translational Research [UL1TR001873]

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Deciphering cell-intrinsic mechanisms of metastasis progression in vivo is essential to identify novel therapeutic approaches. Here we elucidate cell-intrinsic drivers of metastatic prostate cancer progression through analyses of genetically engineered mouse models (GEMM) and correlative studies of human prostate cancer. Expression profiling of lineage-marked cells from mouse primary tumors and metastases defines a signature of de novo metastatic progression. Cross-species master regulator analyses comparing this mouse signature with a comparable human signature identifies conserved drivers of metastatic progression with demonstrable clinical and functional relevance. In particular, nuclear receptor binding SET Domain Protein 2 (NSD2) is robustly expressed in lethal prostate cancer in humans, while its silencing inhibits metastasis of mouse allografts in vivo. We propose that cross-species analysis can elucidate mechanisms of metastasis progression, thus providing potential additional therapeutic opportunities for treatment of lethal prostate cancer.

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