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A Signaling View into the Inflammatory Tumor Microenvironment

2021-06-15Journal article Open access
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dc.contributor.authorPereira, Joana F. S.
dc.contributor.authorJordan, Peter
dc.contributor.authorMatos, Paulo
dc.date.accessioned2022-01-27T16:15:53Z
dc.date.available2022-01-27T16:15:53Z
dc.date.issued2021-06-15
dc.description.abstractThe development of tumors requires an initiator event, usually exposure to DNA damaging agents that cause genetic alterations such as gene mutations or chromosomal abnormalities, leading to deregulated cell proliferation. Although the mere stochastic accumulation of further mutations may cause tumor progression, it is now clear that an inflammatory microenvironment has a major tumor-promoting influence on initiated cells, in particular when a chronic inflammatory reaction already existed before the initiated tumor cell was formed. Moreover, inflammatory cells become mobilized in response to signals emanating from tumor cells. In both cases, the microenvironment provides signals that initiated tumor cells perceive by membrane receptors and transduce via downstream kinase cascades to modulate multiple cellular processes and respond with changes in cell gene expression, metabolism, and morphology. Cytokines, chemokines, and growth factors are examples of major signals secreted by immune cells, fibroblast, and endothelial cells and mediate an intricate cell-cell crosstalk in an inflammatory microenvironment, which contributes to increased cancer cell survival, phenotypic plasticity and adaptation to surrounding tissue conditions. Eventually, consequent changes in extracellular matrix stiffness and architecture, coupled with additional genetic alterations, further fortify the malignant progression of tumor cells, priming them for invasion and metastasis. Here, we provide an overview of the current knowledge on the composition of the inflammatory tumor microenvironment, with an emphasis on the major signals and signal-transducing events mediating different aspects of stromal cell-tumor cell communication that ultimately lead to malignant progression.pt_PT
dc.description.sponsorshipThe work in the authors’ laboratory was supported by Fundação para a Ciência e a Tecnologia (FCT), Portugal, through grant UID/MULTI/04046/2019 to Research Unit BioISI and fellowship SFRH/BD/109162/2015 to JFSP.pt_PT
dc.description.versioninfo:eu-repo/semantics/publishedVersionpt_PT
dc.identifier.citationImmuno. 2021 Jun 15;1(2):91-118. doi: 10.3390/immuno1020007. Reviewpt_PT
dc.identifier.doi10.3390/immuno1020007pt_PT
dc.identifier.issn2673-5601
dc.identifier.urihttp://hdl.handle.net/10400.18/7881
dc.language.isoengpt_PT
dc.peerreviewedyespt_PT
dc.publisherMDPIpt_PT
dc.relationBiosystems & Integrative Sciences Institute
dc.relationEffect of an inflammatory microenvironment on alternative splicing-mediated gene expression plasticity in colorectal cells
dc.relation.publisherversionhttps://www.mdpi.com/2673-5601/1/2/7/htmpt_PT
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/pt_PT
dc.subjectTumor Microenvironmentpt_PT
dc.subjectInflammationpt_PT
dc.subjectSignal Transductionpt_PT
dc.subjectCancerpt_PT
dc.subjectCancropt_PT
dc.subjectInflamaçãopt_PT
dc.subjectMicroambientept_PT
dc.subjectVias de Transdução de Sinal e Patologias Associadaspt_PT
dc.titleA Signaling View into the Inflammatory Tumor Microenvironmentpt_PT
dc.typejournal article
dspace.entity.typePublication
oaire.awardTitleBiosystems & Integrative Sciences Institute
oaire.awardTitleEffect of an inflammatory microenvironment on alternative splicing-mediated gene expression plasticity in colorectal cells
oaire.awardURIinfo:eu-repo/grantAgreement/FCT/6817 - DCRRNI ID/UID%2FMulti%2F04046%2F2019/PT
oaire.awardURIinfo:eu-repo/grantAgreement/FCT//SFRH%2FBD%2F109162%2F2015/PT
oaire.citation.endPage118pt_PT
oaire.citation.issue2pt_PT
oaire.citation.startPage91pt_PT
oaire.citation.titleImmunopt_PT
oaire.citation.volume1pt_PT
oaire.fundingStream6817 - DCRRNI ID
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.embargofctAcesso de acordo com política editorial da revista.pt_PT
rcaap.rightsopenAccesspt_PT
rcaap.typearticlept_PT
relation.isProjectOfPublication35168786-8dfc-4a00-9759-dab3669fe1ae
relation.isProjectOfPublicationa70bea5c-3110-4af1-8e2a-dc548ed7b0e3
relation.isProjectOfPublication.latestForDiscovery35168786-8dfc-4a00-9759-dab3669fe1ae

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