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http://purl.uniprot.org/citations/31841182http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/31841182http://www.w3.org/2000/01/rdf-schema#comment"

Objective

MicroRNA-16 (miR-16) expression has been proved to take part in the initiation and development of several cancers, including hepatocellular carcinoma (HCC). However, its role and its molecular mechanism in HCC cells remain unclear. Our study aimed to elucidate miR-16 probable role and potential mechanism in HCC cells.

Patients and methods

MiR-16 expression in HCC was measured by Real Time-Polymerase Chain Reaction (RT-PCR). MiR-16 mimic or inhibitor was applied to increase or decrease miR-16 expression in Huh7 cells separately. The cell viability was measured by MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide). The invaded cells and migrated cells were detected by the transwell assay. The epithelial-mesenchymal transition (EMT) and the nuclear factor-κB (NF-κB) were performed using Western blot. The tumor growth was measured via xenograft tumor formation assay. Moreover, bioinformatical methods and luciferase reporter assay were carried out to confirm the miR-16 target gene.

Results

MiR-16 expression was downregulated in HCC tissues and cells. Furthermore, the increasing miR-16 expression was suppressed, whereas the decreasing miR-16 expression promoted cell proliferation, invasion, and migration in Huh7 cells. Moreover, miR-16 targeted FEAT in regulating HCC progression. FEAT was associated with a poor prognosis of HCC patients. Especially, miR-16 suppressed EMT and NF-κB pathway in HCC and inhibited the tumor growth in vivo.

Conclusions

We stated that miR-16 suppressed HCC cell progression by targeting FEAT and inhibiting EMT and NF-κB pathway. MiR-16 may be clinically utilized as a factor for the clinical diagnosis and prognosis of HCC."xsd:string
http://purl.uniprot.org/citations/31841182http://purl.org/dc/terms/identifier"doi:10.26355/eurrev_201912_19665"xsd:string
http://purl.uniprot.org/citations/31841182http://purl.uniprot.org/core/author"Li T."xsd:string
http://purl.uniprot.org/citations/31841182http://purl.uniprot.org/core/author"Li N."xsd:string
http://purl.uniprot.org/citations/31841182http://purl.uniprot.org/core/author"Meng F.L."xsd:string
http://purl.uniprot.org/citations/31841182http://purl.uniprot.org/core/author"Chu Y.L."xsd:string
http://purl.uniprot.org/citations/31841182http://purl.uniprot.org/core/author"Gao X.Z."xsd:string
http://purl.uniprot.org/citations/31841182http://purl.uniprot.org/core/author"Su X.F."xsd:string
http://purl.uniprot.org/citations/31841182http://purl.uniprot.org/core/date"2019"xsd:gYear
http://purl.uniprot.org/citations/31841182http://purl.uniprot.org/core/name"Eur Rev Med Pharmacol Sci"xsd:string
http://purl.uniprot.org/citations/31841182http://purl.uniprot.org/core/pages"10274-10282"xsd:string
http://purl.uniprot.org/citations/31841182http://purl.uniprot.org/core/title"MiR-16 inhibits hepatocellular carcinoma progression by targeting FEAT through NF-kappaB signaling pathway."xsd:string
http://purl.uniprot.org/citations/31841182http://purl.uniprot.org/core/volume"23"xsd:string
http://purl.uniprot.org/citations/31841182http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/31841182
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