Tenascin-C Promotes Tumor Cell Migration and Metastasis through Integrin α9β1-Mediated YAP Inhibition.

Fiche publication


Date publication

février 2018

Journal

Cancer research

Auteurs

Membres identifiés du Cancéropôle Est :
Dr LEFEBVRE Olivier, Dr OREND Gertraud


Tous les auteurs :
Sun Z, Schwenzer A, Rupp T, Murdamoothoo D, Vegliante R, Lefebvre O, Klein A, Hussenet T, Orend G

Résumé

Tenascin-C is an extracellular matrix molecule that drives progression of many types of human cancer, but the basis for its actions remains obscure. In this study, we describe a cell-autonomous signaling mechanism explaining how tenascin-C promotes cancer cell migration in the tumor microenvironment. In a murine xenograft model of advanced human osteosarcoma, tenascin-C and its receptor integrin α9β1 were determined to be essential for lung metastasis of tumor cells. We determined that activation of this pathway also reduced tumor cell-autonomous expression of target genes for the transcription factor YAP. In clinical specimens, a genetic signature comprising four YAP target genes represents prognostic impact. Taken together, our results illuminate how tumor cell deposition of tenascin-C in the tumor microenvironment promotes invasive migration and metastatic progression. These results illuminate how the extracellular matrix glycoprotein tenascin-C in the tumor microenvironment promotes invasive migration and metastatic progression by employing integrin α9β1, abolishing actin stress fiber formation, inhibiting YAP and its target gene expression, with potential implications for cancer prognosis and therapy. .

Mots clés

Adaptor Proteins, Signal Transducing, antagonists & inhibitors, Animals, Bone Neoplasms, genetics, Cell Line, Tumor, Cell Movement, physiology, Cell Proliferation, physiology, Heterografts, Humans, Integrins, genetics, Mice, Mice, Nude, Neoplasm Metastasis, Osteosarcoma, genetics, Phosphoproteins, antagonists & inhibitors, Signal Transduction, Tenascin, genetics, Transfection, Tumor Microenvironment

Référence

Cancer Res.. 2018 Feb 15;78(4):950-961