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http://purl.uniprot.org/citations/26309359http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/26309359http://www.w3.org/2000/01/rdf-schema#comment"

Aim

To elucidate the potential biological role of miR-30b in gastric cancer and investigate the underlying molecular mechanisms of miR-30b to inhibit metastasis of gastric cancer cells.

Methods

The expression of miR-30b was detected in gastric cancer cell lines and samples by reverse transcription-polymerase chain reaction. CCK-8 assays were conducted to explore the impact of miR-30b overexpression on the proliferation of gastric cancer cells. Flow cytometry was used to examine the effect of miR-30b on the apoptosis. Transwell test was used for the migration and invasion assays. Luciferase reporter assays and Western blot were employed to validate regulation of putative target of miR-30b.

Results

The results showed that miR-30b was downregulated in gastric cancer tissues and cancer cell lines and functioned as a tumor suppressor. Overexpression of miR-30b promoted cell apoptosis, and suppressed proliferation, migration and invasion of the gastric cancer cell lines AGS and MGC803. Bioinformatic analysis identified the 3'-untranslated region of eukaryotic translation initiation factor 5A2 (EIF5A2) as a putative binding site of miR-30b. Luciferase reporter assays and Western blot analysis confirmed the EIF5A2 gene as a target of miR-30b. Moreover, expression levels of the EIF5A2 targets E-cadherin and Vimentin were altered following transfection of miR-30b mimics.

Conclusion

Our findings describe a link between miR-30b and EIF5A2, which plays an important role in mediating epithelial-mesenchymal transition."xsd:string
http://purl.uniprot.org/citations/26309359http://purl.org/dc/terms/identifier"doi:10.3748/wjg.v21.i31.9337"xsd:string
http://purl.uniprot.org/citations/26309359http://purl.uniprot.org/core/author"Liu Y.Q."xsd:string
http://purl.uniprot.org/citations/26309359http://purl.uniprot.org/core/author"Yan C."xsd:string
http://purl.uniprot.org/citations/26309359http://purl.uniprot.org/core/author"Ye X."xsd:string
http://purl.uniprot.org/citations/26309359http://purl.uniprot.org/core/author"Ma Z.Q."xsd:string
http://purl.uniprot.org/citations/26309359http://purl.uniprot.org/core/author"Yu J.C."xsd:string
http://purl.uniprot.org/citations/26309359http://purl.uniprot.org/core/author"Tian S.B."xsd:string
http://purl.uniprot.org/citations/26309359http://purl.uniprot.org/core/author"Kang W.M."xsd:string
http://purl.uniprot.org/citations/26309359http://purl.uniprot.org/core/date"2015"xsd:gYear
http://purl.uniprot.org/citations/26309359http://purl.uniprot.org/core/name"World J Gastroenterol"xsd:string
http://purl.uniprot.org/citations/26309359http://purl.uniprot.org/core/pages"9337-9347"xsd:string
http://purl.uniprot.org/citations/26309359http://purl.uniprot.org/core/title"MiR-30b suppresses tumor migration and invasion by targeting EIF5A2 in gastric cancer."xsd:string
http://purl.uniprot.org/citations/26309359http://purl.uniprot.org/core/volume"21"xsd:string
http://purl.uniprot.org/citations/26309359http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/26309359
http://purl.uniprot.org/citations/26309359http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/26309359
http://purl.uniprot.org/uniprot/#_Q9GZV4-mappedCitation-26309359http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/26309359
http://purl.uniprot.org/uniprot/Q9GZV4http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/26309359