http://purl.uniprot.org/citations/35468721 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
http://purl.uniprot.org/citations/35468721 | http://www.w3.org/2000/01/rdf-schema#comment | "BackgroundHepatocellular carcinoma (HCC) is a common malignancy. Long non-coding RNAs (lncRNAs) partake in the progression of HCC. However, the role of lncRNA MAPKAPK5-AS1 in the development of HCC has not been fully clarified.MethodsRNA sequencing data and quantitative real-time polymerase chain reaction (qRT-PCR) were adopted to analyze MAPKAPK5-AS1, miR-429 and ZEB1 mRNA expressions in HCC tissues and cell lines. Western blot was used to detect ZEB1, E-cadherin and N-cadherin protein expressions. 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), Transwell and flow cytometry assays were adopted to analyze the effects of MAPKAPK5-AS1 on cell proliferation, migration, invasion and apoptosis. Besides, luciferase reporter assay was used to detect the targeting relationship between miR-429 and MAPKAPK5-AS1 or ZEB1 3'UTR. The xenograft tumor mouse models were used to explore the effect of MAPKAPK5-AS1 on lung metastasis of HCC cells.ResultsMAPKAPK5-AS1 and ZEB1 expressions were up-regulated in HCC tissues, and miR-429 expression is down-regulated in HCC tissues. MAPKAPK5-AS1 knockdown could significantly impede HCC cell proliferation, migration, invasion and epithelial-mesenchymal transition (EMT), as well as promote cell apoptosis. MAPKAPK5-AS1 overexpression could enhance L02 cell proliferation, migration, invasion and EMT, and inhibit cell apoptosis. MiR-429 was validated to be the target of MAPKAPK5-AS1, and miR-429 inhibitors could partially offset the effects of knocking down MAPKAPK5-AS1 on HCC cells. MAPKAPK5-AS1 could positively regulate ZEB1 expression through repressing miR-429. Moreover, fewer lung metastatic nodules were observed in the lung tissues of nude mice when the MAPKAPK5-AS1 was knocked down in HCC cells.ConclusionMAPKAPK5-AS1 can adsorb miR-429 to promote ZEB1 expression to participate in the development of HCC."xsd:string |
http://purl.uniprot.org/citations/35468721 | http://purl.org/dc/terms/identifier | "doi:10.1186/s12860-022-00420-x"xsd:string |
http://purl.uniprot.org/citations/35468721 | http://purl.uniprot.org/core/author | "Wang Y."xsd:string |
http://purl.uniprot.org/citations/35468721 | http://purl.uniprot.org/core/author | "Fan Q."xsd:string |
http://purl.uniprot.org/citations/35468721 | http://purl.uniprot.org/core/author | "Peng Z."xsd:string |
http://purl.uniprot.org/citations/35468721 | http://purl.uniprot.org/core/author | "Ouyang X."xsd:string |
http://purl.uniprot.org/citations/35468721 | http://purl.uniprot.org/core/date | "2022"xsd:gYear |
http://purl.uniprot.org/citations/35468721 | http://purl.uniprot.org/core/name | "BMC Mol Cell Biol"xsd:string |
http://purl.uniprot.org/citations/35468721 | http://purl.uniprot.org/core/pages | "21"xsd:string |
http://purl.uniprot.org/citations/35468721 | http://purl.uniprot.org/core/title | "MAPKAPK5-AS1 drives the progression of hepatocellular carcinoma via regulating miR-429/ZEB1 axis."xsd:string |
http://purl.uniprot.org/citations/35468721 | http://purl.uniprot.org/core/volume | "23"xsd:string |
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