Show simple item record

dc.contributor.authorMuliaditan, Tamara
dc.contributor.authorCaron, Jonathan
dc.contributor.authorOkesola, Mary
dc.contributor.authorOpzoomer, James W
dc.contributor.authorKosti, Paris
dc.contributor.authorGeorgouli, Mirella
dc.contributor.authorGordon, Peter
dc.contributor.authorLall, Sharanpreet
dc.contributor.authorKuzeva, Desislava M
dc.contributor.authorPedro, Luisa
dc.contributor.authorShields, Jacqueline D
dc.contributor.authorGillett, Cheryl E
dc.contributor.authorDiebold, Sandra S
dc.contributor.authorSanz-Moreno, Victoria
dc.contributor.authorNg, Tony
dc.contributor.authorHoste, Esther
dc.contributor.authorArnold, James N
dc.date.accessioned2018-11-07T00:30:49Z
dc.date.available2018-11-07T00:30:49Z
dc.date.issued2018-07-27
dc.identifier.issn2041-1723
dc.identifier.urihttps://www.repository.cam.ac.uk/handle/1810/284694
dc.description.abstractTumour-associated macrophages (TAMs) play an important role in tumour progression, which is facilitated by their ability to respond to environmental cues. Here we report, using murine models of breast cancer, that TAMs expressing fibroblast activation protein alpha (FAP) and haem oxygenase-1 (HO-1), which are also found in human breast cancer, represent a macrophage phenotype similar to that observed during the wound healing response. Importantly, the expression of a wound-like cytokine response within the tumour is clinically associated with poor prognosis in a variety of cancers. We show that co-expression of FAP and HO-1 in macrophages results from an innate early regenerative response driven by IL-6, which both directly regulates HO-1 expression and licenses FAP expression in a skin-like collagen-rich environment. We show that tumours can exploit this response to facilitate transendothelial migration and metastatic spread of the disease, which can be pharmacologically targeted using a clinically relevant HO-1 inhibitor.
dc.format.mediumElectronic
dc.languageeng
dc.publisherSpringer Science and Business Media LLC
dc.rightsAttribution 4.0 International
dc.rights.urihttps://creativecommons.org/licenses/by/4.0/
dc.subjectCell Line, Tumor
dc.subjectMacrophages
dc.subjectSkin
dc.subjectAnimals
dc.subjectMice, Inbred BALB C
dc.subjectHumans
dc.subjectMice
dc.subjectMice, Mutant Strains
dc.subjectBreast Neoplasms
dc.subjectNeoplasm Metastasis
dc.subjectCollagen
dc.subjectGelatinases
dc.subjectSerine Endopeptidases
dc.subjectMembrane Proteins
dc.subjectInterleukin-6
dc.subjectCytokines
dc.subjectPrognosis
dc.subjectWound Healing
dc.subjectCell Survival
dc.subjectGene Expression Regulation, Neoplastic
dc.subjectPhenotype
dc.subjectFemale
dc.subjectHeme Oxygenase-1
dc.subjectTumor Microenvironment
dc.titleMacrophages are exploited from an innate wound healing response to facilitate cancer metastasis.
dc.typeArticle
prism.issueIdentifier1
prism.publicationDate2018
prism.publicationNameNat Commun
prism.startingPage2951
prism.volume9
dc.identifier.doi10.17863/CAM.32067
dcterms.dateAccepted2018-07-03
rioxxterms.versionofrecord10.1038/s41467-018-05346-7
rioxxterms.licenseref.urihttp://www.rioxx.net/licenses/all-rights-reserved
rioxxterms.licenseref.startdate2018-07-27
dc.contributor.orcidSanz-Moreno, Victoria [0000-0002-5096-9456]
dc.contributor.orcidHoste, Esther [0000-0002-3181-431X]
dc.contributor.orcidArnold, James N [0000-0002-6949-0613]
dc.identifier.eissn2041-1723
rioxxterms.typeJournal Article/Review
pubs.funder-project-idMRC (unknown)
pubs.funder-project-idMedical Research Council (MC_UU_12022/5)
cam.issuedOnline2018-07-27


Files in this item

Thumbnail

This item appears in the following Collection(s)

Show simple item record

Attribution 4.0 International
Except where otherwise noted, this item's licence is described as Attribution 4.0 International