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

2017-05-16Journal article Open access
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dc.contributor.authorTavares, Sandra
dc.contributor.authorVieira, André Filipe
dc.contributor.authorTaubenberger, Anna Verena
dc.contributor.authorAraújo, Margarida
dc.contributor.authorMartins, Nuno Pimpao
dc.contributor.authorBrás-Pereira, Catarina
dc.contributor.authorPolónia, António
dc.contributor.authorHerbig, Maik
dc.contributor.authorBarreto, Clara
dc.contributor.authorOtto, Oliver
dc.contributor.authorCardoso, Joana
dc.contributor.authorPereira-Leal, José B.
dc.contributor.authorGuck, Jochen
dc.contributor.authorParedes, Joana
dc.contributor.authorJanody, Florence
dc.date.accessioned2017-05-22T11:38:50Z
dc.date.available2017-05-22T11:38:50Z
dc.date.issued2017-05-16
dc.descriptionThis deposit is composed by the main article and supplementary files of the publication.pt_PT
dc.description.abstractStudies 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.pt_PT
dc.description.sponsorshipBloomington Drosophila Stock Centre; Vienna Drosophila Research Center (VDRC); Developmental Studies Hybridoma Bank (DSHB); Fundação para a Ciência e Tecnologia (FCT) grant: (IF/01031/2012); Laço Grant in breast cancer 2015; Alexander von Humboldt Foundation grant: (Alexander von Humboldt Professorship); Liga Portuguesa contra o Cancro/Pfizer.pt_PT
dc.description.versioninfo:eu-repo/semantics/publishedVersionpt_PT
dc.identifier.citationTavares, S. et al. Actin stress fiber organization promotes cell stiffening and proliferation of pre-invasive breast cancer cells. Nat. Commun. 8, 15237 doi: 10.1038/ncomms15237 (2017).pt_PT
dc.identifier.doi10.1038/ncomms15237pt_PT
dc.identifier.urihttp://hdl.handle.net/10400.7/756
dc.language.isoengpt_PT
dc.peerreviewedyespt_PT
dc.publisherNature Publishing Grouppt_PT
dc.relationIF/01031/2012pt_PT
dc.relationLaço Grant in breast cancer 2015pt_PT
dc.relationSTUDY OF THE CROSS-TALK BETWEEN THE SRC PROTO-ONCOGENE AND F-ACTIN DURING TUMOURAL TRANSFORMATION
dc.relationLiga Portuguesa contra o Cancro/Pfizerpt_PT
dc.relation.publisherversionhttps://www.nature.com/articles/ncomms15237pt_PT
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/pt_PT
dc.subjectBiophysicspt_PT
dc.subjectCancerpt_PT
dc.subjectCytoskeletonpt_PT
dc.titleActin stress fiber organization promotes cell stiffening and proliferation of pre-invasive breast cancer cellspt_PT
dc.typejournal article
dspace.entity.typePublication
oaire.awardTitleSTUDY OF THE CROSS-TALK BETWEEN THE SRC PROTO-ONCOGENE AND F-ACTIN DURING TUMOURAL TRANSFORMATION
oaire.awardURIinfo:eu-repo/grantAgreement/FCT/3599-PPCDT/PTDC%2FBIA-BCM%2F121455%2F2010/PT
oaire.awardURIinfo:eu-repo/grantAgreement/FCT//SFRH%2FBD%2F51884%2F2012/PT
oaire.citation.endPage18pt_PT
oaire.citation.startPage1pt_PT
oaire.citation.titleNature Communicationspt_PT
oaire.citation.volume8pt_PT
oaire.fundingStream3599-PPCDT
project.funder.identifierhttp://doi.org/10.13039/501100001871
project.funder.identifierhttp://doi.org/10.13039/501100001871
project.funder.nameFundação para a Ciência e a Tecnologia
project.funder.nameFundação para a Ciência e a Tecnologia
rcaap.rightsopenAccesspt_PT
rcaap.typearticlept_PT
relation.isProjectOfPublicationd5de197b-f2b9-4534-acba-416206be7fa0
relation.isProjectOfPublication92418758-eaf1-47a5-9fd9-5c9da6d745aa
relation.isProjectOfPublication.latestForDiscovery92418758-eaf1-47a5-9fd9-5c9da6d745aa

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