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Bacterial genotoxins promote inside-out integrin β1 activation, formation of focal adhesion complexes and cell spreading
Department of Cell and Molecular Biology, Karolinska Institutet, Stockholm, Sweden. (Teresa Frisan)ORCID-id: 0000-0002-1209-0942
2015 (Engelska)Ingår i: PLoS ONE, ISSN 1932-6203, E-ISSN 1932-6203, Vol. 10, nr 4, artikel-id e0124119Artikel i tidskrift (Refereegranskat) Published
Abstract [en]

Integrins are membrane bound receptors that regulate several cellular processes, such as cell adhesion, migration, survival and proliferation, and may contribute to tumor initiation/progression in cells exposed to genotoxic stress. The extent of integrin activation and its role in cell survival upon intoxication with bacterial genotoxins are still poorly characterized. These toxins induce DNA strand breaks in the target cells and activate the DNA damage response (DDR), coordinated by the Ataxia Telangectasia Mutated (ATM) kinase. In the present study, we demonstrate that induction of DNA damage by two bacterial genotoxins promotes activation of integrin β1, leading to enhanced assembly of focal adhesions and cell spreading on fibronectin, but not on vitronectin. This phenotype is mediated by an ATM-dependent inside-out integrin signaling, and requires the actin cytoskeleton remodeler NET1. The toxin-mediated cell spreading and anchorage-independent survival further relies on ALIX and TSG101, two components of the endosomal sorting complex required for transport (ESCRT), known to regulate integrin intracellular trafficking. These data reveal a novel aspect of the cellular response to bacterial genotoxins, and provide new tools to understand the carcinogenic potential of these effectors in the context of chronic intoxication and infection.

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Public Library Science , 2015. Vol. 10, nr 4, artikel-id e0124119
Nationell ämneskategori
Cellbiologi Immunologi Mikrobiologi Cell- och molekylärbiologi Cancer och onkologi
Identifikatorer
URN: urn:nbn:se:umu:diva-165080DOI: 10.1371/journal.pone.0124119ISI: 000352845100240PubMedID: 25874996OAI: oai:DiVA.org:umu-165080DiVA, id: diva2:1369405
Tillgänglig från: 2019-11-12 Skapad: 2019-11-12 Senast uppdaterad: 2019-11-12Bibliografiskt granskad

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CellbiologiImmunologiMikrobiologiCell- och molekylärbiologiCancer och onkologi

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