Show simple item record

dc.contributor.advisorWood, Stephen
dc.contributor.advisorMeedeniya, Adrian
dc.contributor.authorAlowaidi, Faisal A N
dc.date.accessioned2018-01-23T02:27:44Z
dc.date.available2018-01-23T02:27:44Z
dc.date.issued2015
dc.identifier.doi10.25904/1912/2709
dc.identifier.urihttp://hdl.handle.net/10072/366238
dc.description.abstractGlioblastoma multiforme (GBM) is one of the most aggressive tumours and has poor survival rate. The expression of the embryonic stem cell factor Crypto-1 has been documented in most cancer types. More specifically, Cripto-1 expression has recently been correlated with low survival rate of young glioblastoma patients. It has been demonstrated that Cripto-1 controls cell survival and stemness, as well as proliferation and epithelial to mesenchymal transition (EMT). The contribution of Cripto-1 to tumour vascularisation was also reported. Even though Cripto-1 expression and signalling in most cancers has been well characterised, its involvement in controlling glioblastoma cells is poorly studied. The aim of this thesis was to interrogate the contribution of Cripto-1 to multiple processes mediating gliomagenesis and further to understand the underlying signalling pathways impacted upon by Cripto-1. The findings of the current study are in line with those reported for other tumour models. Moreover, this study provides further evidence on the important roles Cripto-1 plays in tumourigenesis, particularly, its role in de-differentiating cancer cells. This was shown by confirming its effect on the activation of factors known to maintain cancer cells in an undifferentiated state like OCT4, NANOG and SOX2. Most significantly, this study has unravelled for the first time the positive effect of ectopic Cripto-1 expression on CD44, a cell surface marker known for its involvement in maintaining GBM stem like cells in their undifferentiated phenotype. We also show that Cripto-1 is indispensable in controlling the infiltrative phenotype of glioma cells via regulating EMT. Ectopic Cripto-1 expression also regulates the proliferation of this GBM cell model by increasing levels of the proliferation markers Ki-67 and cyclin D1. This led to a significant increase in cellular growth rate over time. These findings suggest that Cripto-1 might control cellular proliferation in GBM.
dc.languageEnglish
dc.publisherGriffith University
dc.publisher.placeBrisbane
dc.rights.copyrightThe author owns the copyright in this thesis, unless stated otherwise.
dc.subject.keywordsGlioblastoma multiforme (GBM)
dc.subject.keywordsCrypto-1
dc.subject.keywordsStem cells
dc.subject.keywordsTumours
dc.titleFunctional Identification of Cripto-1 (TDGF1) Role in Glioblastoma Multiforme
dc.typeGriffith thesis
dc.date.embargoEnd2018
gro.facultyGriffith Health
gro.description.notepublicIn order to comply with copyright the following figures have not been published here: Figures 1.1, 1.2, 1.3, 1.4, 1.5, 4.2, 4.3, 4.4.
gro.rights.copyrightThe author owns the copyright in this thesis, unless stated otherwise.
gro.hasfulltextFull Text
dc.contributor.otheradvisorIvanovski, Saso
dc.contributor.otheradvisorBellette, Bernadette
gro.identifier.gurtIDgu1447717737998
gro.source.ADTshelfnoADT0
gro.source.GURTshelfnoGURT
gro.thesis.degreelevelThesis (PhD Doctorate)
gro.thesis.degreeprogramDoctor of Philosophy (PhD)
gro.departmentSchool of Medical Science
gro.griffith.authorAlowaidi, Faisal


Files in this item

This item appears in the following Collection(s)

Show simple item record