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NSD2 is a conserved driver of metastatic prostate cancer progression

Author

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  • Alvaro Aytes

    (Columbia University Irving Medical Center
    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)

  • Arianna Giacobbe

    (Columbia University Irving Medical Center
    Columbia University Irving Medical Center)

  • Antonina Mitrofanova

    (Columbia University Irving Medical Center
    The State University of New Jersey)

  • 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
    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
    University of Bern)

  • Michael M. Shen

    (Columbia University Irving Medical Center
    Columbia University Irving Medical Center
    Columbia University Irving Medical Center
    Columbia University Irving Medical Center)

  • Andrea Califano

    (Columbia University Irving Medical Center
    Columbia University Irving Medical Center
    Columbia University Irving Medical Center)

  • Cory Abate-Shen

    (Columbia University Irving Medical Center
    Columbia University Irving Medical Center
    Columbia University Irving Medical Center
    Columbia University Irving Medical Center)

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.

Suggested Citation

  • 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 & Cory Aba, 2018. "NSD2 is a conserved driver of metastatic prostate cancer progression," Nature Communications, Nature, vol. 9(1), pages 1-14, December.
    • Handle: RePEc:nat:natcom:v:9:y:2018:i:1:d:10.1038_s41467-018-07511-4
    DOI: 10.1038/s41467-018-07511-4
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