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

Zhen Sun1,2,3,4, Anja Schwenzer1,2,3,4, Tristan Rupp1,2,3,4

  • 1INSERM U1109 - MN3T, The Microenvironmental Niche in Tumorigenesis and Targeted Therapy, Hôpital Civil, Institut d'Hématologie et d'Immunologie, Strasbourg, France.

Cancer Research
|December 21, 2017
PubMed

Insights

Tenascin-C promotes cancer metastasis by activating integrin α9β1, which inhibits YAP signaling. This mechanism explains how tenascin-C drives tumor cell migration and progression in the tumor microenvironment.

Area of Science:

  • Oncology
  • Molecular Biology
  • Extracellular Matrix Biology

Background:

  • Tenascin-C is an extracellular matrix protein implicated in cancer progression.
  • The precise mechanisms by which tenascin-C influences cancer cell behavior are not fully understood.

Purpose of the Study:

  • To elucidate the cell-autonomous signaling pathway through which tenascin-C promotes cancer cell migration.
  • To investigate the role of tenascin-C and its receptor integrin α9β1 in osteosarcoma metastasis.

Main Methods:

  • Utilized a murine xenograft model of human osteosarcoma.
  • Assessed the expression and function of tenascin-C and integrin α9β1.
  • Analyzed the impact on YAP target gene expression and actin stress fiber formation.

Main Results:

  • Tenascin-C and integrin α9β1 were essential for lung metastasis in osteosarcoma.
  • Activation of the tenascin-C/integrin α9β1 pathway reduced YAP target gene expression.
  • This pathway was linked to reduced actin stress fiber formation.

Conclusions:

  • Tenascin-C promotes invasive migration and metastasis through integrin α9β1-mediated inhibition of YAP signaling.
  • A YAP target gene signature has prognostic implications in clinical cancer specimens.
  • These findings offer potential therapeutic targets for inhibiting cancer progression.

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