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Article

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Accepted version

Publication date

2017-03-01

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Please use this identifier to cite or link to this item: https://hdl.handle.net/2445/120671

A mechanically active heterotypic E-cadherin/N-cadherin adhesion enables fibroblasts to drive cancer cell invasion

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https://doi.org/10.1038/ncb3478

Abstract

Cancer-associated fibroblasts (CAFs) promote tumour invasion and metastasis. We show that CAFs exert a physical force on cancer cells that enables their collective invasion. Force transmission is mediated by a heterophilic adhesion involving N-cadherin at the CAF membrane and E-cadherin at the cancer cell membrane. This adhesion is mechanically active; when subjected to force it triggers β-catenin recruitment and adhesion reinforcement dependent on α-catenin/vinculin interaction. Impairment of E-cadherin/N-cadherin adhesion abrogates the ability of CAFs to guide collective cell migration and blocks cancer cell invasion. N-cadherin also mediates repolarization of the CAFs away from the cancer cells. In parallel, nectins and afadin are recruited to the cancer cell/CAF interface and CAF repolarization is afadin dependent. Heterotypic junctions between CAFs and cancer cells are observed in patient-derived material. Together, our findings show that a mechanically active heterophilic adhesion between CAFs and cancer cells enables cooperative tumour invasion.

Subject

Fibroblasts, Tumors, Patologia cel·lular

Subject (English)

Fibroblasts, Tumors, Cellular pathology

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Articles publicats en revistes (Biomedicina)
Articles publicats en revistes (Institut de Bioenginyeria de Catalunya (IBEC))

Citation

LABERNADIE, Anna, et al. A mechanically active heterotypic E-cadherin/N-cadherin adhesion enables fibroblasts to drive cancer cell invasion. Nature Cell Biology. 2017. Vol. 19, num. 3, pags. 224-237. ISSN 1465-7392. [consulted: 12 of August of 2026]. Available at: https://hdl.handle.net/2445/120671

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