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dc.rights.licenseopenen_US
hal.structure.identifierChimie et Biologie des Membranes et des Nanoobjets [CBMN]
dc.contributor.authorGOUNOU, Celine
hal.structure.identifierChimie et Biologie des Membranes et des Nanoobjets [CBMN]
dc.contributor.authorBOUVET, Flora
hal.structure.identifierBoRdeaux Institute in onCology [Inserm U1312 - BRIC]
dc.contributor.authorLIET, Benjamin
hal.structure.identifierBoRdeaux Institute in onCology [Inserm U1312 - BRIC]
dc.contributor.authorPROUZET-MAULEON, Valerie
hal.structure.identifierChimie et Biologie des Membranes et des Nanoobjets [CBMN]
dc.contributor.authorD'AGATA, Lena
hal.structure.identifierLaboratoire Ondes et Matière d'Aquitaine [LOMA]
dc.contributor.authorHARTE, Etienne
hal.structure.identifierLaboratoire Ondes et Matière d'Aquitaine [LOMA]
dc.contributor.authorARGOUL, Francoise
hal.structure.identifierBoRdeaux Institute in onCology [Inserm U1312 - BRIC]
dc.contributor.authorSIEGFRIED, Geraldine
hal.structure.identifierBoRdeaux Institute in onCology [Inserm U1312 - BRIC]
dc.contributor.authorIGGO, Richard
hal.structure.identifierBoRdeaux Institute in onCology [Inserm U1312 - BRIC]
dc.contributor.authorKHATIB, Abdel‐majid
hal.structure.identifierChimie et Biologie des Membranes et des Nanoobjets [CBMN]
dc.contributor.authorBOUTER, Anthony
dc.date.accessioned2024-04-24T09:00:50Z
dc.date.available2024-04-24T09:00:50Z
dc.date.issued2023-04-07
dc.identifier.issn0248-4900en_US
dc.identifier.urihttps://oskar-bordeaux.fr/handle/20.500.12278/199293
dc.description.abstractEnAbstract Background Information During tumor invasion and metastasis processes, cancer cells are exposed to major compressive and shearing forces, due to their migration through extracellular matrix, dense cell areas, and complex fluids, which may lead to numerous plasma membrane damages. Cancer cells may survive to these mechanical stresses thanks to an efficient membrane repair machinery. Consequently, this machinery may constitute a relevant target to inhibit cancer cell dissemination. Results We show here that annexin‐A5 (ANXA5) and ANXA6 participate in membrane repair of MDA‐MB‐231 cells, a highly invasive triple‐negative breast cancer cell line. These crucial components of the membrane repair machinery are substantially expressed in breast cancer cells in correlation with their invasive properties. In addition, high expression of ANXA5 and ANXA6 predict poor prognosis in high‐grade lung, gastric, and breast cancers. In zebrafish, the genetic inhibition of ANXA5 and ANXA6 leads to drastic reduction of tumor cell dissemination. Conclusion We conclude that the inhibition of ANXA5 and ANXA6 prevents membrane repair in cancer cells, which are thus unable to survive to membrane damage during metastasis. Significance This result opens a new therapeutic strategy based on targeting membrane repair machinery to inhibit tumor invasion and metastasis.
dc.language.isoENen_US
dc.rights.urihttp://creativecommons.org/licenses/by/
dc.title.enAnnexin‐A5 and annexin‐A6 silencing prevents metastasis of breast cancer cells in zebrafish
dc.typeArticle de revueen_US
dc.identifier.doi10.1111/boc.202200110en_US
dc.subject.halSciences du Vivant [q-bio]en_US
dc.subject.halPhysique [physics]en_US
bordeaux.journalBiology of the Cellen_US
bordeaux.volume115en_US
bordeaux.hal.laboratoriesCBMN : Chimie & de Biologie des Membranes & des Nano-objets - UMR 5248en_US
bordeaux.issue6en_US
bordeaux.institutionUniversité de Bordeauxen_US
bordeaux.institutionBordeaux INPen_US
bordeaux.institutionCNRSen_US
bordeaux.peerReviewedouien_US
bordeaux.inpressnonen_US
bordeaux.import.sourcehal
hal.identifierhal-04305236
hal.version1
hal.popularnonen_US
hal.audienceInternationaleen_US
hal.exportfalse
workflow.import.sourcehal
dc.rights.ccPas de Licence CCen_US
bordeaux.COinSctx_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.jtitle=Biology%20of%20the%20Cell&rft.date=2023-04-07&rft.volume=115&rft.issue=6&rft.eissn=0248-4900&rft.issn=0248-4900&rft.au=GOUNOU,%20Celine&BOUVET,%20Flora&LIET,%20Benjamin&PROUZET-MAULEON,%20Valerie&D'AGATA,%20Lena&rft.genre=article


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