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2017-03-01

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Si us plau utilitzeu sempre aquest identificador per citar o enllaçar aquest document: 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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Recurs relacionat

https://doi.org/10.1038/ncb3478

Resum

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.

Matèries

Fibroblasts, Tumors, Patologia cel·lular

Matèries (anglès)

Fibroblasts, Tumors, Cellular pathology

Citació

Col·leccions

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

Citació

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: 15 of August of 2026]. Available at: https://hdl.handle.net/2445/120671

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