NSD2 is a conserved driver of metastatic prostate cancer progression

Alvaro Aytes (), Arianna Giacobbe, Antonina Mitrofanova, Katia Ruggero, Joanna Cyrta, Juan Arriaga, Luis Palomero, Sonia Farran-Matas, Mark A. Rubin, Michael M. Shen, Andrea Califano () and Cory Abate-Shen ()
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Alvaro Aytes: Columbia University Irving Medical Center
Arianna Giacobbe: Columbia University Irving Medical Center
Antonina Mitrofanova: Columbia University Irving Medical Center
Katia Ruggero: Programs of Molecular Mechanisms and Experimental Therapeutics in Oncology (ONCOBell), and Cancer Therapeutics Resistance (ProCURE), Catalan Institute of Oncology, Bellvitge Institute for Biomedical Research, L’Hospitalet de Llobregat
Joanna Cyrta: Weill Cornell Medicine
Juan Arriaga: Columbia University Irving Medical Center
Luis Palomero: Programs of Molecular Mechanisms and Experimental Therapeutics in Oncology (ONCOBell), and Cancer Therapeutics Resistance (ProCURE), Catalan Institute of Oncology, Bellvitge Institute for Biomedical Research, L’Hospitalet de Llobregat
Sonia Farran-Matas: Programs of Molecular Mechanisms and Experimental Therapeutics in Oncology (ONCOBell), and Cancer Therapeutics Resistance (ProCURE), Catalan Institute of Oncology, Bellvitge Institute for Biomedical Research, L’Hospitalet de Llobregat
Mark A. Rubin: Weill Cornell Medicine
Michael M. Shen: Columbia University Irving Medical Center
Andrea Califano: Columbia University Irving Medical Center
Cory Abate-Shen: Columbia University Irving Medical Center

Nature Communications, 2018, vol. 9, issue 1, 1-14

Abstract: Abstract 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.

Date: 2018
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DOI: 10.1038/s41467-018-07511-4

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