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http://purl.uniprot.org/citations/30575904http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
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Objective

The aim of this study was to explore the role of microRNA-210 (miR-210) and E2F3 in the development of pancreatic cancer and to investigate the possible underlying mechanism.

Patients and methods

The expression level of miR-210 in pancreatic cancer tissues, para-cancerous tissues, and normal pancreatic tissues was detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). The correlation between miR-210 expression and pathological indicators of pancreatic cancer was analyzed. Meanwhile, the expression of miR-210 in pancreatic cancer cells and normal pancreatic ductal epithelial cells was detected by qRT-PCR. After transfection with miR-210 mimics and inhibitor, the viability and cell cycle of pancreatic cancer cells were detected by cell counting kit-8 (CCK-8) assay and flow cytometry, respectively. The binding condition of miR-210 and E2F3 was verified by Dual-Luciferase reporter gene assay.

Results

MiR-210 was lowly expressed in pancreatic cancer tissues than that of para-cancerous tissues. The expression of miR-210 was negatively correlated with TNM stage and tumor size of pancreatic cancer. In vitro experiments showed that the miR-210 was downregulated in pancreatic cancer cells than that of normal pancreatic ductal epithelial cells. Meanwhile, overexpression of miR-210 arrested cell cycle decreased cell viability and downregulated E2F3 expression in pancreatic cancer cells. Dual-Luciferase reporter gene assay indicated that E2F3 bound to mi-210. Further experiments confirmed that E2F3 was negatively regulated by miR-210.

Conclusions

MiR-210 knockdown promotes cell proliferation by upregulating E2F3 expression, thereby promoting the progression of pancreatic cancer."xsd:string
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http://purl.uniprot.org/citations/30575904http://purl.uniprot.org/core/author"Han B."xsd:string
http://purl.uniprot.org/citations/30575904http://purl.uniprot.org/core/author"Gao J."xsd:string
http://purl.uniprot.org/citations/30575904http://purl.uniprot.org/core/author"Lin Y."xsd:string
http://purl.uniprot.org/citations/30575904http://purl.uniprot.org/core/author"Li S.J."xsd:string
http://purl.uniprot.org/citations/30575904http://purl.uniprot.org/core/author"Zhang C.S."xsd:string
http://purl.uniprot.org/citations/30575904http://purl.uniprot.org/core/author"Sun F.B."xsd:string
http://purl.uniprot.org/citations/30575904http://purl.uniprot.org/core/date"2018"xsd:gYear
http://purl.uniprot.org/citations/30575904http://purl.uniprot.org/core/name"Eur Rev Med Pharmacol Sci"xsd:string
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http://purl.uniprot.org/citations/30575904http://purl.uniprot.org/core/title"MiR-210 knockdown promotes the development of pancreatic cancer via upregulating E2F3 expression."xsd:string
http://purl.uniprot.org/citations/30575904http://purl.uniprot.org/core/volume"22"xsd:string
http://purl.uniprot.org/citations/30575904http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/30575904
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