http://purl.uniprot.org/citations/27518872 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
http://purl.uniprot.org/citations/27518872 | http://www.w3.org/2000/01/rdf-schema#comment | "MicroRNAs (miRNAs) have been widely accepted as a class of gene expression regulators which post-translationally regulate protein expression. These small noncoding RNAs have been proved closely involved in the modulation of various pathobiological processes in cancer. In this research, we demonstrated that miR-148a expression was significantly down-regulated in gastric cancer tissues in comparison with the matched normal mucosal tissues, and its expression was statistically associated with lymph node metastasis. Ectopic expression of miR-148a inhibited tumor cell proliferation and migration in vitro, and inhibited tumor formation in vivo. Subsequently, we identified cholecystokinin B receptor (CCK-BR) as a direct target of miR-148a using western blot and luciferase activity assay. More importantly, siRNA-induced knockdown of CCK-BR elicited similar anti-oncogenic effects (decreased proliferation and migration) as those induced by enforced miR-148a expression. We also found that miR-148a-mediated anti-cancer effects are dependent on the inhibition of STAT3 and Akt activation, which subsequently regulates the pathways involved in cell proliferation and migration. Taken together, our results suggest that miR-148a serves as a tumor suppressor in human gastric carcinogenesis by targeting CCK-BR via inactivating STAT3 and Akt."xsd:string |
http://purl.uniprot.org/citations/27518872 | http://purl.org/dc/terms/identifier | "doi:10.1371/journal.pone.0158961"xsd:string |
http://purl.uniprot.org/citations/27518872 | http://purl.uniprot.org/core/author | "Liu B."xsd:string |
http://purl.uniprot.org/citations/27518872 | http://purl.uniprot.org/core/author | "Li J."xsd:string |
http://purl.uniprot.org/citations/27518872 | http://purl.uniprot.org/core/author | "Gu Q."xsd:string |
http://purl.uniprot.org/citations/27518872 | http://purl.uniprot.org/core/author | "Yu Y."xsd:string |
http://purl.uniprot.org/citations/27518872 | http://purl.uniprot.org/core/author | "Zhu Z."xsd:string |
http://purl.uniprot.org/citations/27518872 | http://purl.uniprot.org/core/author | "Yu B."xsd:string |
http://purl.uniprot.org/citations/27518872 | http://purl.uniprot.org/core/author | "Su L."xsd:string |
http://purl.uniprot.org/citations/27518872 | http://purl.uniprot.org/core/author | "Yan M."xsd:string |
http://purl.uniprot.org/citations/27518872 | http://purl.uniprot.org/core/author | "Lv X."xsd:string |
http://purl.uniprot.org/citations/27518872 | http://purl.uniprot.org/core/date | "2016"xsd:gYear |
http://purl.uniprot.org/citations/27518872 | http://purl.uniprot.org/core/name | "PLoS One"xsd:string |
http://purl.uniprot.org/citations/27518872 | http://purl.uniprot.org/core/pages | "e0158961"xsd:string |
http://purl.uniprot.org/citations/27518872 | http://purl.uniprot.org/core/title | "MiR-148a Functions as a Tumor Suppressor by Targeting CCK-BR via Inactivating STAT3 and Akt in Human Gastric Cancer."xsd:string |
http://purl.uniprot.org/citations/27518872 | http://purl.uniprot.org/core/volume | "11"xsd:string |
http://purl.uniprot.org/citations/27518872 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/27518872 |
http://purl.uniprot.org/citations/27518872 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/27518872 |
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http://purl.uniprot.org/uniprot/#_A0SEH5-mappedCitation-27518872 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/27518872 |
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http://purl.uniprot.org/uniprot/#_A0SEH7-mappedCitation-27518872 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/27518872 |