期刊
NATURE COMMUNICATIONS
卷 9, 期 -, 页码 -出版社
NATURE PORTFOLIO
DOI: 10.1038/s41467-018-07511-4
关键词
-
资金
- Flow Cytometry Core
- JP Sulzberger Columbia Genome Center
- Small Animal Imaging Facility
- NIH/NCI [P30 CA013696]
- National Cancer Institute [CA173481, CA196662, U54 CA209997, P50 CA211024, R35 CA197745]
- TJ Martell Foundation for Leukemia, Cancer and AIDS Research
- Instituto de Salut Carlos III [PI16/01070, CP15/00090]
- European Association of Urology Research Foundation [EAURF/407003/XH]
- Fundacion BBVA
- CERCA Program/Generalitat de Catalunya
- FEDER funds/European Regional Development Fund (ERDF)-a way to Build Europe
- DOD Prostate Cancer Research Program [PC150959, PC141549]
- International Cancer Research Fellowship Outgoing - Associazione Italiana per la Ricerca sul Cancro (AIRC)
- Marie Curie Actions COFUND
- Department of Defense Award [W81XWH-18-1-0193]
- Nuovo-Soldati Foundation
- Irving Institute/Clinical Trials Office (CTO) Pilot Award [UR002765-01]
- Irving Institute for Clinical and Translational Research [UL1TR001873]
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.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据