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http://purl.uniprot.org/citations/35963185http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/35963185http://www.w3.org/2000/01/rdf-schema#comment"

Background

Biological mechanism of miR-210-3p in endometrial carcinoma (EC) remains unclear. Here, our purpose is to study effects of miR-210-3p on malignant progression of EC.

Methods

Bioinformatics analysis showed miRNA and mRNA are abnormally expressed in EC tissues. Quantitative real-time fluorescence polymerase chain reaction (qRT-PCR) was utilized to compare miR-210-3p mRNA level in EC cells and tissues. qRT-PCR and western blot were used to measure RUNX1T1 and NCAM1 at mRNA and protein levels, and western blot for p-AKT and AKT proteins related to PI3K/AKT signaling pathway. Furthermore, EC cell behaviors were assayed via Cell Counting Kit-8, cell colony formation assay, wound healing, transwell and flow cytometry experiments. Interaction between RUNX1T1 and miR-210-3p was verified through dual-luciferase assay. Immunohistochemistry was used to analyze RUNX1T1 expression in clinical samples RESULTS: MiR-210-3p was considerably upregulated and RUNX1T1 was significantly under-expressed in EC. Overexpression of miR-210-3p stimulated cell proliferation, migration, invasion, and restrained cell apoptosis in EC. Dual-luciferase assay proved that RUNX1T1 was a target gene of miR-210-3p. The level of RUNX1T1 in EC was downregulated after overexpressing miR-210-3p. Rescue assay showed that overexpression of RUNX1T1 had an inhibitory impact on tumor-relevant cell behaviors, whereas overexpression of miR-210-3p rescued such inhibition. Overexpression of RUNX1T1 reduced p-AKT expression, which was restored with concomitantly overexpressed miR-210-3p.

Conclusion

In general, miR-210-3p behaves as an oncogene in EC by down-regulating the expression of RUNX1T1. This study elucidates a new functional mechanism in EC, and indicates miR-210-3p an underlying target."xsd:string
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http://purl.uniprot.org/citations/35963185http://purl.uniprot.org/core/author"Chen J."xsd:string
http://purl.uniprot.org/citations/35963185http://purl.uniprot.org/core/author"Li L."xsd:string
http://purl.uniprot.org/citations/35963185http://purl.uniprot.org/core/author"Luo H."xsd:string
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http://purl.uniprot.org/citations/35963185http://purl.uniprot.org/core/pages"111793"xsd:string
http://purl.uniprot.org/citations/35963185http://purl.uniprot.org/core/title"MiR-210-3p accelerates tumor-relevant cell functions of endometrial carcinoma by repressing RUNX1T1."xsd:string
http://purl.uniprot.org/citations/35963185http://purl.uniprot.org/core/volume"825"xsd:string
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