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dc.contributor.authorAlowaidi, Faisal
dc.contributor.authorHashimi, Saeed M
dc.contributor.authorAlqurashi, Naif
dc.contributor.authorWood, Stephen A
dc.contributor.authorWei, Ming Q
dc.date.accessioned2019-12-13T03:38:58Z
dc.date.available2019-12-13T03:38:58Z
dc.date.issued2019
dc.identifier.issn1792-1074
dc.identifier.doi10.3892/ol.2019.10626
dc.identifier.urihttp://hdl.handle.net/10072/389782
dc.description.abstractDiscovering the underlying signalling pathways that control cancer cells is crucial for understanding their biology and to develop therapeutic regimens. Thus, the aim of the present study was to determine the effect of Cripto‑1 on pathways controlling glioblastoma (GBM) cell function. To this end, changes in protein phosphorylation in cells overexpressing Cripto‑1 were analysed using the Kyoto Encyclopedia of Genes and Genomes pathway analysis tool, as well as the Uniprot resource to identify the functions of Cripto‑1‑dependent phosphorylated proteins. This revealed that proteins affected by Cripto‑1 overexpression are involved in multiple signalling pathways. The mitogen‑activated protein kinase (MAPK), focal adhesion (FA) and ErbB pathways were found to be enriched by Cripto‑1 overexpression with 35, 27 and 24% of pathway proteins phosphorylated, respectively. These pathways control important cellular processes in cancer cells that correlate with the observed functional changes described in earlier studies. More specifically, Cripto‑1 may regulate MAPK cellular proliferation and survival pathways by activating epithelial growth factor receptor (EGFR; Ser1070) or fibroblast GFR1 (Tyr654). Its effect on cellular proliferation and survival could be mediated through Src (Tyr418), FA kinase (FAK; Tyr396), p130CAS (Tyr410), c‑Jun (Ser63), Paxillin (PXN; Tyr118) and BCL2 (Thr69) of the FA pathway. Cripto‑1 may also control cellular motility and invasion by activating Src (Tyr418), FAK (Tyr396) and PXN (Tyr118) of the FA pathway. However, Cripto‑1 regulation of cellular invasion and migration might be not limited to the FA pathway, it may also control these cellular mechanisms through signalling via EGFR (Ser1070)/Her2 (Tyr877) to mediate the Src (Tyr418) and FAK (Tyr396) cascade activation of the ErbB signalling pathway. Angiogenesis could be mediated by Cripto‑1 by activating c‑Jun (Ser63) through EGFR (Ser1070)/Her2 (Tyr877) of the ErbB pathway. To conclude, the present study has augmented and enriched our current knowledge on the crucial roles that Cripto‑1 may play in controlling different cellular mechanisms in GBM cells.
dc.description.peerreviewedYes
dc.languageEnglish
dc.language.isoeng
dc.publisherSpandidos Publications
dc.relation.ispartofpagefrom3399
dc.relation.ispartofpageto3406
dc.relation.ispartofissue3
dc.relation.ispartofjournalOncology Letters
dc.relation.ispartofvolume18
dc.subject.fieldofresearchOncology and carcinogenesis
dc.subject.fieldofresearchcode3211
dc.subject.keywordsScience & Technology
dc.subject.keywordsLife Sciences & Biomedicine
dc.subject.keywordsOncology
dc.subject.keywordssignalling pathways
dc.subject.keywordsphosphoproteome
dc.titleCripto-1 overexpression in U87 glioblastoma cells activates MAPK, focal adhesion and ErbB pathways
dc.typeJournal article
dc.type.descriptionC1 - Articles
dcterms.bibliographicCitationAlowaidi, F; Hashimi, SM; Alqurashi, N; Wood, SA; Wei, MQ, Cripto-1 overexpression in U87 glioblastoma cells activates MAPK, focal adhesion and ErbB pathways, Oncology Letters, 2019, 18 (3), pp. 3399-3406
dcterms.dateAccepted2019-06-17
dcterms.licensehttps://creativecommons.org/licenses/by-nc-nd/4.0/
dc.date.updated2019-12-13T03:32:31Z
dc.description.versionVersion of Record (VoR)
gro.rights.copyright© The Author(s) 2019. This is an open access article distributed under the terms of Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0) License, which permits unrestricted, non-commercial use, distribution and reproduction in any medium, providing that the work is properly cited.
gro.hasfulltextFull Text
gro.griffith.authorWei, Ming Q.


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