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dc.contributor.authorViloria, K
dc.contributor.authorMunasinghe, A
dc.contributor.authorAsher, S
dc.contributor.authorBogyere, R
dc.contributor.authorJones, L
dc.contributor.authorHill, NJ
dc.date.accessioned2021-08-13T10:23:35Z
dc.date.available2021-08-13T10:23:35Z
dc.date.issued2016
dc.identifier.issn2045-2322
dc.identifier.issn2045-2322
dc.identifier.other37839
dc.identifier.urihttp://hdl.handle.net/10026.1/17580
dc.description.abstract

<jats:title>Abstract</jats:title><jats:p>SPARC is a matricellular protein that is involved in both pancreatic cancer and diabetes. It belongs to a wider family of proteins that share structural and functional similarities. Relatively little is known about this extended family, but evidence of regulatory interactions suggests the importance of a holistic approach to their study. We show that Hevin, SPOCKs, and SMOCs are strongly expressed within islets, ducts, and blood vessels, suggesting important roles for these proteins in the normal pancreas, while FSTL-1 expression is localised to the stromal compartment reminiscent of SPARC. In direct contrast to SPARC, however, FSTL-1 expression is reduced in pancreatic cancer. Consistent with this, FSTL-1 inhibited pancreatic cancer cell proliferation. The complexity of SPARC family proteins is further revealed by the detection of multiple cell-type specific isoforms that arise due to a combination of post-translational modification and alternative splicing. Identification of splice variants lacking a signal peptide suggests the existence of novel intracellular isoforms. This study underlines the importance of addressing the complexity of the SPARC family and provides a new framework to explain their controversial and contradictory effects. We also demonstrate for the first time that FSTL-1 suppresses pancreatic cancer cell growth.</jats:p>

dc.format.extent37839-
dc.format.mediumElectronic
dc.languageen
dc.language.isoeng
dc.publisherSpringer Science and Business Media LLC
dc.subjectAlternative Splicing
dc.subjectAnimals
dc.subjectCalcium-Binding Proteins
dc.subjectCell Line, Tumor
dc.subjectCell Proliferation
dc.subjectDown-Regulation
dc.subjectExtracellular Matrix Proteins
dc.subjectFollistatin-Related Proteins
dc.subjectGene Expression Regulation, Neoplastic
dc.subjectHumans
dc.subjectIslets of Langerhans
dc.subjectMice
dc.subjectNeoplasm Transplantation
dc.subjectPancreatic Neoplasms
dc.subjectProtein Processing, Post-Translational
dc.subjectProteoglycans
dc.titleA holistic approach to dissecting SPARC family protein complexity reveals FSTL-1 as an inhibitor of pancreatic cancer cell growth
dc.typejournal-article
dc.typeArticle
plymouth.author-urlhttps://www.ncbi.nlm.nih.gov/pubmed/27886258
plymouth.issue1
plymouth.volume6
plymouth.publisher-urlhttp://dx.doi.org/10.1038/srep37839
plymouth.publication-statusPublished online
plymouth.journalScientific Reports
dc.identifier.doi10.1038/srep37839
plymouth.organisational-group/Plymouth
plymouth.organisational-group/Plymouth/Faculty of Health
plymouth.organisational-group/Plymouth/Faculty of Health/School of Biomedical Sciences
plymouth.organisational-group/Plymouth/Users by role
plymouth.organisational-group/Plymouth/Users by role/Academics
dc.publisher.placeEngland
dcterms.dateAccepted2016-11-02
dc.identifier.eissn2045-2322
dc.rights.embargoperiodNot known
rioxxterms.versionofrecord10.1038/srep37839
rioxxterms.licenseref.urihttp://www.rioxx.net/licenses/all-rights-reserved
rioxxterms.licenseref.startdate2016-11-25
rioxxterms.typeJournal Article/Review


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