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Please use this identifier to cite or link to this item: https://hdl.handle.net/10216/145270
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dc.creatorMaia, J
dc.creatorOtake, AH
dc.creatorPoças, J
dc.creatorCarvalho, AS
dc.creatorBeck, HC
dc.creatorMagalhães, A
dc.creatorMatthiesen, R
dc.creatorStrano Moraes, MC
dc.creatorCosta-Silva, B
dc.date.accessioned2022-11-17T11:33:11Z-
dc.date.available2022-11-17T11:33:11Z-
dc.date.issued2020
dc.identifier.issn2296-634X
dc.identifier.urihttps://hdl.handle.net/10216/145270-
dc.description.abstractPancreatic cancers (PC) are highly metastatic with poor prognosis, mainly due to delayed detection. We previously showed that PC-derived extracellular vesicles (EVs) act on macrophages residing in the liver, eliciting extracellular matrix remodeling in this organ and marked hepatic accumulation of CD11b+ bone marrow (BM) cells, which support PC liver metastasis. We here show that PC-EVs also bind to CD11b+ BM cells and induce the expansion of this cell population. Transcriptomic characterization of these cells shows that PC-EVs upregulate IgG and IgA genes, which have been linked to the presence of monocytes/macrophages in tumor microenvironments. We also report here the transcriptional downregulation of genes linked to monocyte/macrophage activation, trafficking, and expression of inflammatory molecules. Together, these results show for the first time the existence of a PC–BM communication axis mediated by EVs with a potential role in PC tumor microenvironments.
dc.description.sponsorshipJM was supported by “Fundação para a Ciência e a Tecnologia” (PD/BD/105866/2014). This work was supported by the Champalimaud Foundation; grant 751547 from H2020-MSCA-IF-2016; EMBO Installation Grant 3921; grant 2017NovPCC1058 from Breast Cancer Now’s Catalyst Programme, which is supported by funding from Pfizer; grant 765492 from H2020-MSCA-ITN-2017; and grant LCF/PR/HR19/52160014 from “La Caixa” Foundation. This work was also funded by FEDER funds through the Operational Programme for Competitiveness Factors-COMPETE and National Funds through the Foundation for Science and Technology (FCT), under the project: PTDC/MED-ONC/28489/2017 (to AM). JP acknowledges the FCT grant SFRH/BD/137319/2018.
dc.language.isoeng
dc.publisherFrontiers Media
dc.relationinfo:eu-repo/grantAgreement/FCT/OE/PD%2FBD%2F105866%2F2014/PT
dc.relationinfo:eu-repo/grantAgreement/FCT/9471 - RIDTI/PTDC%2FMED-ONC%2F28489%2F2017/PT
dc.relationinfo:eu-repo/grantAgreement/FCT/POR_NORTE/SFRH%2FBD%2F137319%2F2018/PT
dc.relation.ispartofFrontiers in Cell and Developmental Biology, vol.8:592518
dc.rightsopenAccess
dc.rights.urihttps://creativecommons.org/licenses/by/4.0/
dc.subjectCancer
dc.subjectExosomes
dc.subjectExtracellular vesicles
dc.subjectMacrophages
dc.subjectMetastasis
dc.subjectMonocytes
dc.subjectPancreatic cancer
dc.subjectTumor microenvironment
dc.titleTranscriptome Reprogramming of CD11b(+) Bone Marrow Cells by Pancreatic Cancer Extracellular Vesicles
dc.typeArtigo em Revista Científica Internacional
dc.contributor.uportoInstituto de Investigação e Inovação em Saúde
dc.identifier.doi10.3389/fcell.2020.592518
dc.relation.publisherversionhttps://www.frontiersin.org/articles/10.3389/fcell.2020.592518/full
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