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http://purl.uniprot.org/citations/35468721http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/35468721http://www.w3.org/2000/01/rdf-schema#comment"

Background

Hepatocellular 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.

Methods

RNA 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.

Results

MAPKAPK5-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.

Conclusion

MAPKAPK5-AS1 can adsorb miR-429 to promote ZEB1 expression to participate in the development of HCC."xsd:string
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http://purl.uniprot.org/citations/35468721http://purl.uniprot.org/core/author"Wang Y."xsd:string
http://purl.uniprot.org/citations/35468721http://purl.uniprot.org/core/author"Fan Q."xsd:string
http://purl.uniprot.org/citations/35468721http://purl.uniprot.org/core/author"Peng Z."xsd:string
http://purl.uniprot.org/citations/35468721http://purl.uniprot.org/core/author"Ouyang X."xsd:string
http://purl.uniprot.org/citations/35468721http://purl.uniprot.org/core/date"2022"xsd:gYear
http://purl.uniprot.org/citations/35468721http://purl.uniprot.org/core/name"BMC Mol Cell Biol"xsd:string
http://purl.uniprot.org/citations/35468721http://purl.uniprot.org/core/pages"21"xsd:string
http://purl.uniprot.org/citations/35468721http://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/35468721http://purl.uniprot.org/core/volume"23"xsd:string
http://purl.uniprot.org/citations/35468721http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/35468721
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