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dc.contributor.authorVosgha, Haleh
dc.contributor.authorAriana, Armin
dc.contributor.authorSmith, Robert Anthony
dc.contributor.authorLam, Alfred King-yin
dc.date.accessioned2019-05-29T13:05:19Z
dc.date.available2019-05-29T13:05:19Z
dc.date.issued2018
dc.identifier.issn1351-0088
dc.identifier.doi10.1530/ERC-17-0497
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.
dc.description.peerreviewedYes
dc.languageEnglish
dc.publisherSociety for Endrocrinology
dc.publisher.placeUnited Kingdom
dc.relation.ispartofpagefrom323
dc.relation.ispartofpageto337
dc.relation.ispartofissue3
dc.relation.ispartofjournalEndocrine-Related Cancer
dc.relation.ispartofvolume25
dc.subject.fieldofresearchMedical and Health Sciences not elsewhere classified
dc.subject.fieldofresearchMedical and Health Sciences
dc.subject.fieldofresearchBiological Sciences
dc.subject.fieldofresearchcode119999
dc.subject.fieldofresearchcode11
dc.subject.fieldofresearchcode06
dc.titlemiR-205 targets angiogenesis and EMT concurrently in anaplastic thyroid carcinoma
dc.typeJournal article
dc.type.descriptionC1 - Articles
dc.type.codeC - Journal Articles
dc.description.versionPost-print
gro.facultyGriffith Health, School of Medicine
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.
gro.hasfulltextFull Text
gro.griffith.authorSmith, Robert A.
gro.griffith.authorLam, Alfred K.
gro.griffith.authorAriana, Armin S.
gro.griffith.authorVosgha, Haleh


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