| http://purl.uniprot.org/citations/28800788 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/28800788 | http://www.w3.org/2000/01/rdf-schema#comment | "MicroRNAs (miRNAs) are small noncoding RNAs that are involved in human carcinogenesis and progression. miR-204 has been reported to be a tumor suppressor in several cancer types. However, the function and underlying molecular mechanism of miR-204 in cervical cancer (CC) are still unclear. In the present study, the expression level of miR-204 was measured using the qRT-PCR method in 30 paired CC clinical samples and in 6 CC cell lines. We found that the expression of miR-204 was significantly downregulated in CC tissues and cell lines compared to normal cervical tissues and cell line. miR-204 was overexpressed by transfection with the miR-204 mimic in HeLa and C33A cell lines in the following experiments. The results showed that overexpression of miR-204 dramatically suppressed cell proliferation, migration, and invasion, caused cell cycle arrest at the G0/G1 phase, promoted cell apoptosis in vitro, and inhibited tumor growth in vivo. Western blot results indicated that overexpressing miR-204 decreased the expressions of CDK2, cyclin E, MMP2, MMP9, Bcl2, whereas it enhanced Bax expression and suppressed the activation of the PI3K/AKT signaling pathways in CC cells. Ephrin type B receptor 2 (EphB2) was identified as a direct target of miR-204 in CC cells according to bioinformatics analysis and luciferase reporter assay. Furthermore, knockdown of EphB2 mimicked the inhibitory effect of miR-204 on the proliferation, invasion, and migration of CC cells. These findings suggested that miR-204 might serve as a tumor suppressor in the development of CC by directly targeting EphB2."xsd:string |
| http://purl.uniprot.org/citations/28800788 | http://purl.org/dc/terms/identifier | "doi:10.3727/096504017x15016337254641"xsd:string |
| http://purl.uniprot.org/citations/28800788 | http://purl.uniprot.org/core/author | "Chen Z."xsd:string |
| http://purl.uniprot.org/citations/28800788 | http://purl.uniprot.org/core/author | "Liu L."xsd:string |
| http://purl.uniprot.org/citations/28800788 | http://purl.uniprot.org/core/author | "Duan S."xsd:string |
| http://purl.uniprot.org/citations/28800788 | http://purl.uniprot.org/core/author | "Yang Y."xsd:string |
| http://purl.uniprot.org/citations/28800788 | http://purl.uniprot.org/core/author | "Wu A."xsd:string |
| http://purl.uniprot.org/citations/28800788 | http://purl.uniprot.org/core/author | "Shu Q."xsd:string |
| http://purl.uniprot.org/citations/28800788 | http://purl.uniprot.org/core/date | "2018"xsd:gYear |
| http://purl.uniprot.org/citations/28800788 | http://purl.uniprot.org/core/name | "Oncol Res"xsd:string |
| http://purl.uniprot.org/citations/28800788 | http://purl.uniprot.org/core/pages | "713-723"xsd:string |
| http://purl.uniprot.org/citations/28800788 | http://purl.uniprot.org/core/title | "miR-204 Regulates Cell Proliferation and Invasion by Targeting EphB2 in Human Cervical Cancer."xsd:string |
| http://purl.uniprot.org/citations/28800788 | http://purl.uniprot.org/core/volume | "26"xsd:string |
| http://purl.uniprot.org/citations/28800788 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/28800788 |
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