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http://purl.uniprot.org/citations/32432752http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/32432752http://www.w3.org/2000/01/rdf-schema#comment"

Objective

Various microRNAs (miRNAs) have been reported to be involved in the pathogenesis and development of human cancers, including papillary thyroid carcinoma (PTC). However, the role of miR-224-5p in PTC progression remains unclear. Therefore, the purpose of this study is to illuminate the function of miR-224-5p in PTC.

Patients and methods

Expression of miR-224-5p and EGR2 was examined in PTC by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). Transwell assay was used to detect cell migration and invasion. Western blot analysis was used to detect epithelial-mesenchymal transition (EMT). The relationship between miR-224-5p and EGR2 was confirmed by Dual-Luciferase assay.

Results

Upregulation of miR-224-5p and downregulation of EGR2 expression were detected in PTC tissues and cells. Upregulation of miR-224-5p was found to be associated with TNM stage and lymph node metastasis. Meanwhile, it also predicted poor prognosis in PTC patients. Functionally, upregulation of miR-224-5p promoted cell metastasis and EMT in PTC. In addition, miR-224-5p was detected to directly target EGR2. EGR2 expression was negatively correlated with EGR2 expression in PTC. Of note, overexpression of EGR2 attenuated the carcinogenic effects of miR-224-5p in PTC.

Conclusions

MiR-224-5p promotes cell migration, invasion, and EMT in PTC by targeting EGR2."xsd:string
http://purl.uniprot.org/citations/32432752http://purl.org/dc/terms/identifier"doi:10.26355/eurrev_202005_21178"xsd:string
http://purl.uniprot.org/citations/32432752http://purl.uniprot.org/core/author"Qiu J."xsd:string
http://purl.uniprot.org/citations/32432752http://purl.uniprot.org/core/author"Sun J."xsd:string
http://purl.uniprot.org/citations/32432752http://purl.uniprot.org/core/author"Huang H.T."xsd:string
http://purl.uniprot.org/citations/32432752http://purl.uniprot.org/core/author"Jiang L.W."xsd:string
http://purl.uniprot.org/citations/32432752http://purl.uniprot.org/core/author"Zang C.S."xsd:string
http://purl.uniprot.org/citations/32432752http://purl.uniprot.org/core/author"Ge R.F."xsd:string
http://purl.uniprot.org/citations/32432752http://purl.uniprot.org/core/date"2020"xsd:gYear
http://purl.uniprot.org/citations/32432752http://purl.uniprot.org/core/name"Eur Rev Med Pharmacol Sci"xsd:string
http://purl.uniprot.org/citations/32432752http://purl.uniprot.org/core/pages"4890-4900"xsd:string
http://purl.uniprot.org/citations/32432752http://purl.uniprot.org/core/title"MiR-224-5p targets EGR2 to promote the development of papillary thyroid carcinoma."xsd:string
http://purl.uniprot.org/citations/32432752http://purl.uniprot.org/core/volume"24"xsd:string
http://purl.uniprot.org/citations/32432752http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/32432752
http://purl.uniprot.org/citations/32432752http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/32432752
http://purl.uniprot.org/uniprot/#_P11161-mappedCitation-32432752http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/32432752
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http://purl.uniprot.org/uniprot/#_B4DL38-mappedCitation-32432752http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/32432752
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http://purl.uniprot.org/uniprot/B4DL38http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/32432752
http://purl.uniprot.org/uniprot/P11161http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/32432752
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