| http://purl.uniprot.org/citations/32324847 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/32324847 | http://www.w3.org/2000/01/rdf-schema#comment | "Hepatocellular carcinoma (HCC) is one of the most lethal cancers in the world. MicroRNAs play a pivotal role in the progression of various cancers. To date, very little attention has been paid to miR-4458. Therefore, the aim of our study was to explore the function and underlying molecular mechanism of miR-4458 in HCC. We found that the expression of miR-4458 was reduced in HCC tissues and cell lines. Forced overexpression of miR-4458 inhibited the migration, invasion, and epithelial-mesenchymal transition (EMT) of HCC cells, while downregulation of miR-4458 promoted the aggressive phenotype. Furthermore, transforming growth factor beta receptor 1 (TGFBR1), the modulator of the TGF-β signaling pathway, was verified to be a novel target gene of miR-4458 by dual-luciferase reporter gene assay. Upregulated miR-4458 dramatically abolished TGFBR1 and p-Smad2/3 expression, thus blocking the TGF-β signaling pathway. Moreover, restoration of TGFBR1 partially rescued the miR-4458-mediated suppressive effect on the migration, invasion, and EMT and reactivated the TGF-β signaling pathway in HCC cells. In summary, our findings first demonstrated a mechanism of miR-4458 in HCC cell migration, invasion, and EMT by regulating the TGF-β signaling pathway via directly targeting TGFBR1."xsd:string |
| http://purl.uniprot.org/citations/32324847 | http://purl.org/dc/terms/identifier | "doi:10.1093/abbs/gmaa029"xsd:string |
| http://purl.uniprot.org/citations/32324847 | http://purl.uniprot.org/core/author | "Chen W."xsd:string |
| http://purl.uniprot.org/citations/32324847 | http://purl.uniprot.org/core/author | "Liu H."xsd:string |
| http://purl.uniprot.org/citations/32324847 | http://purl.uniprot.org/core/author | "Luo Y."xsd:string |
| http://purl.uniprot.org/citations/32324847 | http://purl.uniprot.org/core/author | "Zhang Y."xsd:string |
| http://purl.uniprot.org/citations/32324847 | http://purl.uniprot.org/core/author | "Shi K."xsd:string |
| http://purl.uniprot.org/citations/32324847 | http://purl.uniprot.org/core/author | "Wei X."xsd:string |
| http://purl.uniprot.org/citations/32324847 | http://purl.uniprot.org/core/author | "Wu Z."xsd:string |
| http://purl.uniprot.org/citations/32324847 | http://purl.uniprot.org/core/date | "2020"xsd:gYear |
| http://purl.uniprot.org/citations/32324847 | http://purl.uniprot.org/core/name | "Acta Biochim Biophys Sin (Shanghai)"xsd:string |
| http://purl.uniprot.org/citations/32324847 | http://purl.uniprot.org/core/pages | "554-562"xsd:string |
| http://purl.uniprot.org/citations/32324847 | http://purl.uniprot.org/core/title | "miR-4458 inhibits the epithelial-mesenchymal transition of hepatocellular carcinoma cells by suppressing the TGF-beta signaling pathway via targeting TGFBR1."xsd:string |
| http://purl.uniprot.org/citations/32324847 | http://purl.uniprot.org/core/volume | "52"xsd:string |
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