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http://purl.uniprot.org/citations/28618953http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/28618953http://www.w3.org/2000/01/rdf-schema#comment"The epithelial-mesenchymal transition is the key process driving cancer metastasis. MicroRNA-194 inhibits epithelial-mesenchymal transition in several cancers and its downregulation indicates a poor prognosis in human endometrial carcinoma. Self-renewal factor Sox3 induces epithelial-mesenchymal transition at gastrulation and is also involved epithelial-mesenchymal transition in several cancers. We intended to determine the roles of Sox3 in inducing epithelial-mesenchymal transition in endometrial cancer stem cells and the possible role of microRNA-194 in controlling Sox3 expression. Firstly, we found that Sox3 and microRNA-194 expressions were associated with the status of endometrial cancer stem cells in a panel of endometrial carcinoma tissue, the CD133+ cell was higher in tumorsphere than in differentiated cells, and overexpression of microRNA-194 would decrease CD133+ cell expression. Silencing of Sox3 in endometrial cancer stem cell upregulated the epithelial marker E-cadherin, downregulated the mesenchymal marker vimentin, and significantly reduced cell invasion in vitro; overexpression of Sox3 reversed these phenotypes. Furthermore, we discovered that the expression of Sox3 was suppressed by microRNA-194 through direct binding to the Sox3 3'-untranslated region. Ectopic expression of microRNA-194 in endometrial cancer stem cells induced a mesenchymal-epithelial transition by restoring E-cadherin expression, decreasing vimentin expression, and inhibiting cell invasion in vitro. Moreover, overexpression of microRNA-194 inhibited endometrial cancer stem cell invasion or metastasis in vivo by injection of adenovirus microRNA-194. These findings demonstrate the novel mechanism by which Sox3 contributes to endometrial cancer stem cell invasion and suggest that repression of Sox3 by microRNA-194 may have therapeutic potential to suppress endometrial carcinoma metastasis. The cancer stem cell marker, CD133, might be the surface marker of endometrial cancer stem cell."xsd:string
http://purl.uniprot.org/citations/28618953http://purl.org/dc/terms/identifier"doi:10.1177/1010428317706217"xsd:string
http://purl.uniprot.org/citations/28618953http://purl.uniprot.org/core/author"Jin Q."xsd:string
http://purl.uniprot.org/citations/28618953http://purl.uniprot.org/core/author"Zhang Y."xsd:string
http://purl.uniprot.org/citations/28618953http://purl.uniprot.org/core/author"Zhou X."xsd:string
http://purl.uniprot.org/citations/28618953http://purl.uniprot.org/core/author"Wang R."xsd:string
http://purl.uniprot.org/citations/28618953http://purl.uniprot.org/core/author"Yue Y."xsd:string
http://purl.uniprot.org/citations/28618953http://purl.uniprot.org/core/author"Gong B."xsd:string
http://purl.uniprot.org/citations/28618953http://purl.uniprot.org/core/date"2017"xsd:gYear
http://purl.uniprot.org/citations/28618953http://purl.uniprot.org/core/name"Tumour Biol"xsd:string
http://purl.uniprot.org/citations/28618953http://purl.uniprot.org/core/pages"1010428317706217"xsd:string
http://purl.uniprot.org/citations/28618953http://purl.uniprot.org/core/title"Overexpression of microRNA-194 suppresses the epithelial-mesenchymal transition in targeting stem cell transcription factor Sox3 in endometrial carcinoma stem cells."xsd:string
http://purl.uniprot.org/citations/28618953http://purl.uniprot.org/core/volume"39"xsd:string
http://purl.uniprot.org/citations/28618953http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/28618953
http://purl.uniprot.org/citations/28618953http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/28618953
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http://purl.uniprot.org/uniprot/#_A0A0A0N0N1-mappedCitation-28618953http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/28618953
http://purl.uniprot.org/uniprot/#_Q15505-mappedCitation-28618953http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/28618953
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http://purl.uniprot.org/uniprot/#_B0AZU8-mappedCitation-28618953http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/28618953
http://purl.uniprot.org/uniprot/#_B3KQS1-mappedCitation-28618953http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/28618953
http://purl.uniprot.org/uniprot/#_P41225-mappedCitation-28618953http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/28618953
http://purl.uniprot.org/uniprot/#_O43490-mappedCitation-28618953http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/28618953
http://purl.uniprot.org/uniprot/O43490http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/28618953