Actin stress fiber organization promotes cell stiffening and proliferation of pre-invasive breast cancer cells

Sandra Tavares, André Filipe Vieira, Anna Verena Taubenberger, Margarida Araújo, Nuno Pimpao Martins, Catarina Brás-Pereira, António Polónia, Maik Herbig, Clara Barreto, Oliver Otto, Joana Cardoso, José B. Pereira-Leal, Jochen Guck, Joana Paredes and Florence Janody ()
Additional contact information
Sandra Tavares: Instituto Gulbenkian de Ciência, Rua da Quinta Grande 6
André Filipe Vieira: Epithelial Interactions in Cancer group, Instituto de Investigação e Inovação em Saúde (i3S), Universidade do Porto
Anna Verena Taubenberger: Biotechnology Center, Technische Universität Dresden
Margarida Araújo: Instituto Gulbenkian de Ciência, Rua da Quinta Grande 6
Nuno Pimpao Martins: Instituto Gulbenkian de Ciência, Rua da Quinta Grande 6
Catarina Brás-Pereira: Instituto Gulbenkian de Ciência, Rua da Quinta Grande 6
António Polónia: Epithelial Interactions in Cancer group, Instituto de Investigação e Inovação em Saúde (i3S), Universidade do Porto
Maik Herbig: Biotechnology Center, Technische Universität Dresden
Clara Barreto: Instituto Gulbenkian de Ciência, Rua da Quinta Grande 6
Oliver Otto: Biotechnology Center, Technische Universität Dresden
Joana Cardoso: Instituto Gulbenkian de Ciência, Rua da Quinta Grande 6
José B. Pereira-Leal: Instituto Gulbenkian de Ciência, Rua da Quinta Grande 6
Jochen Guck: Biotechnology Center, Technische Universität Dresden
Joana Paredes: Epithelial Interactions in Cancer group, Instituto de Investigação e Inovação em Saúde (i3S), Universidade do Porto
Florence Janody: Instituto Gulbenkian de Ciência, Rua da Quinta Grande 6

Nature Communications, 2017, vol. 8, issue 1, 1-18

Abstract: Abstract Studies of the role of actin in tumour progression have highlighted its key contribution in cell softening associated with cell invasion. Here, using a human breast cell line with conditional Src induction, we demonstrate that cells undergo a stiffening state prior to acquiring malignant features. This state is characterized by the transient accumulation of stress fibres and upregulation of Ena/VASP-like (EVL). EVL, in turn, organizes stress fibres leading to transient cell stiffening, ERK-dependent cell proliferation, as well as enhancement of Src activation and progression towards a fully transformed state. Accordingly, EVL accumulates predominantly in premalignant breast lesions and is required for Src-induced epithelial overgrowth in Drosophila. While cell softening allows for cancer cell invasion, our work reveals that stress fibre-mediated cell stiffening could drive tumour growth during premalignant stages. A careful consideration of the mechanical properties of tumour cells could therefore offer new avenues of exploration when designing cancer-targeting therapies.

Date: 2017
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DOI: 10.1038/ncomms15237

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