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dc.contributor.authorVosgha, Halehen_US
dc.contributor.authorAriana, Arminen_US
dc.contributor.authorSmith, Roberten_US
dc.contributor.authorLam, Alfreden_US
dc.date.accessioned2019-05-29T13:05:19Z
dc.date.available2019-05-29T13:05:19Z
dc.date.issued2018en_US
dc.identifier.issn1351-0088en_US
dc.identifier.doi10.1530/ERC-17-0497en_US
dc.identifier.urihttp://hdl.handle.net/10072/380192
dc.description.abstractThe current study aims to evaluate for the first time the inhibitory roles of miR-205 in the pathogenesis of anaplastic thyroid carcinoma. In addition, we investigated the mechanisms by which miR-205 regulates angiogenesis and epithelial-to-mesenchymal transition (EMT) in cancer. Two anaplastic thyroid carcinoma cell lines were transfected with the expression vector pCMV-MIR-205. Selected markers of angiogenesis and EMT including vascular endothelial growth factor A (VEGF-A) and zinc finger E-box-binding homeobox 1 (ZEB1) were investigated by Western blot. The interaction of miR-205 expression with EMT and angiogenesis were also investigated by assessment of matrix metalloproteinases 2 and 9 (MMP2 and MMP 9), SNAI1 (Snai1 family zinc finger 1), vimentin, E-cadherin and N-cadherin. The function of miR-205 was further tested with VEGF enzyme-linked immunosorbent assay (ELISA), wound healing, invasion and tube formation assays. Using an animal model, we studied the association of miR-205 with angiogenesis, proliferation and invasion. The following results were obtained. Permanent overexpression of miR-205 significantly suppressed angiogenesis and EMT by simultaneously targeting VEGF-A, ZEB1 and downstream products. Ectopic expression of miR-205 in cancer cells led to decreased migration, invasion and tube formation of endothelial cells. In addition, inhibition of tumour growth, vascularisation and invasion were noted in the mouse tumour xenografts. Our findings provide insights into simultaneous regulatory role of miR-205 in the pathogenesis of anaplastic thyroid carcinoma by suppressing both angiogenesis and EMT. This may open avenues to exploit miR-205 as an alternative cancer therapeutic strategy in the future.en_US
dc.description.peerreviewedYesen_US
dc.languageEnglishen_US
dc.publisherSociety for Endrocrinologyen_US
dc.publisher.placeUnited Kingdomen_US
dc.relation.ispartofpagefrom323en_US
dc.relation.ispartofpageto337en_US
dc.relation.ispartofissue3en_US
dc.relation.ispartofjournalEndocrine-Related Canceren_US
dc.relation.ispartofvolume25en_US
dc.subject.fieldofresearchMedical and Health Sciences not elsewhere classifieden_US
dc.subject.fieldofresearchMedical and Health Sciencesen_US
dc.subject.fieldofresearchBiological Sciencesen_US
dc.subject.fieldofresearchcode119999en_US
dc.subject.fieldofresearchcode11en_US
dc.subject.fieldofresearchcode06en_US
dc.titlemiR-205 targets angiogenesis and EMT concurrently in anaplastic thyroid carcinomaen_US
dc.typeJournal articleen_US
dc.type.descriptionC1 - Articlesen_US
dc.type.codeC - Journal Articlesen_US
dc.description.versionPost-printen_US
gro.facultyGriffith Health, School of Medicineen_US
gro.rights.copyrightDisclaimer. This is not the definitive version of record of this article. This manuscript has been accepted for publication in Endocrine-Related Cancer, but the version presented here has not yet been copy edited, formatted or proofed. Consequently, the Society for Endocrinology accepts no responsibility for any errors or omissions it may contain. Copyright 2018 Society for Endocrinology. Please refer to the journal's website for access to the definitive, published version.en_US
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