| http://purl.uniprot.org/citations/36190397 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/36190397 | http://www.w3.org/2000/01/rdf-schema#comment | "Gastric cancer (GC) is a subtype of a common malignant tumor found in the digestive system. Hsa_circ_0006470 is known to be closely associated with the development of GC. Nevertheless, the mechanism by which hsa_circ_0006470 regulates the tumorigenesis of GC has not been fully elucidated. To investigate the role of hsa_circ_0006470 in GC, its expression levels were assessed in GES-1, AGS, MKN45, and SNU5 cells by reverse transcription-quantitative PCR. Fluorescence in situ hybridization was used to evaluate the localization of hsa_circ_0006470 in AGS and MKN45 cells. In addition, cell counting kit-8 and 5-ethynyl-2'-deoxyuridine assays were performed to evaluate the viability and proliferation of GC cells, respectively. The dual-luciferase reporter assay was used to explore the interaction among hsa_circ_0006470, microRNA (miR)-1234, and TP53I11. The expression levels of TP53I11, Akt, p-Akt, forkhead box O1, and cyclin dependent kinase 2 in AGS cells were analyzed by Western blotting. The data indicated that hsa_circ_0006470 expression was downregulated in AGS cells. In addition, overexpression (OE) of hsa_circ_0006470 could inhibit the viability and proliferation of GC cells. Moreover, OE of hsa_circ_0006470 inhibited the migration of GC cells and induced G1 cell cycle phase arrest. Moreover, miR-1234 was bound to hsa_circ_0006470 and TP53I11 was targeted by miR-1234. Furthermore, OE of hsa_circ_0006470 inhibited the tumorigenesis of GC via the regulation of the miR-1234/TP53I11 axis. In summary, the present study demonstrated that OE of hsa_circ_0006470 notably inhibited the tumorigenesis of GC by regulating the miR-1234/TP53I11 axis. Therefore, the present study may provide a theoretical basis for exploring novel therapeutic strategies for the treatment of GC."xsd:string |
| http://purl.uniprot.org/citations/36190397 | http://purl.org/dc/terms/identifier | "doi:10.4081/ejh.2022.3477"xsd:string |
| http://purl.uniprot.org/citations/36190397 | http://purl.uniprot.org/core/author | "Guo R."xsd:string |
| http://purl.uniprot.org/citations/36190397 | http://purl.uniprot.org/core/author | "Lin Y."xsd:string |
| http://purl.uniprot.org/citations/36190397 | http://purl.uniprot.org/core/author | "Wang S."xsd:string |
| http://purl.uniprot.org/citations/36190397 | http://purl.uniprot.org/core/author | "Zhang L."xsd:string |
| http://purl.uniprot.org/citations/36190397 | http://purl.uniprot.org/core/author | "Xie J."xsd:string |
| http://purl.uniprot.org/citations/36190397 | http://purl.uniprot.org/core/author | "Ning Y."xsd:string |
| http://purl.uniprot.org/citations/36190397 | http://purl.uniprot.org/core/date | "2022"xsd:gYear |
| http://purl.uniprot.org/citations/36190397 | http://purl.uniprot.org/core/name | "Eur J Histochem"xsd:string |
| http://purl.uniprot.org/citations/36190397 | http://purl.uniprot.org/core/title | "Overexpression of hsa_circ_0006470 inhibits the malignant behavior of gastric cancer cells via regulation of miR-1234/TP53I11 axis."xsd:string |
| http://purl.uniprot.org/citations/36190397 | http://purl.uniprot.org/core/volume | "66"xsd:string |
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