| http://purl.uniprot.org/citations/35193469 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/35193469 | http://www.w3.org/2000/01/rdf-schema#comment | "The oncogenic role of actin filament-associated protein 1 antisense RNA 1 (AFAP1-AS1) has been reported in retinoblastoma (RB). However, the underlying regulatory mechanisms remain poorly understood. In this study, reverse transcription-quantitative polymerase chain reaction (RT-qPCR) and Western blotting were performed to analyze the expression of AFAP1-AS1, microRNA miR-545-3p, or G protein subunit beta 1 (GNB1). Cell Counting Kit-8 (CCK-8) and Transwell migration assays were used to detect cell proliferation and migration. In addition, caspase-3 activity was monitored by caspase-3 activity assay. Luciferase reporter assays combined with RNA immunoprecipitation (RIP) and pull-down assays were performed to elucidate the target relationship between miR-545-3p and AFAP1-AS1 or GNB1. Xenograft tumor experiments were performed to evaluate RB cell growth in vivo. Increased AFAP1-AS1 and GNB1 expression in RB tissues and cells was confirmed by RT-qPCR; conversely, miR-545-3p was found to be downregulated in RB tissues and cells. AFAP1-AS1 overexpression resulted in increased proliferation and migration of RB cells, whereas AFAP1-AS1 silencing resulted in decreased proliferation and migration of RB cells. Moreover, AFAP1-AS1 was found to target miR-545-3p. The anti-miR-545-3p treatment phenocopied the effect of AFAP1-AS1 overexpression and promoted RB cell growth in vivo. miR-545-3p was found to directly target GNB1. GNB1 silencing resulted in reduced proliferation and migration of RB cells and attenuated the oncogenic effect of the miR-545-3p inhibitor. Thus, in this study, a novel ceRNA regulation network of AFAP1-AS1 in RB was identified, where AFAP1-AS1 regulated GNB1 expression by targeting miR-545-3p, ultimately driving RB progression."xsd:string |
| http://purl.uniprot.org/citations/35193469 | http://purl.org/dc/terms/identifier | "doi:10.1080/21655979.2022.2033464"xsd:string |
| http://purl.uniprot.org/citations/35193469 | http://purl.uniprot.org/core/author | "Guan Y."xsd:string |
| http://purl.uniprot.org/citations/35193469 | http://purl.uniprot.org/core/author | "Li J."xsd:string |
| http://purl.uniprot.org/citations/35193469 | http://purl.uniprot.org/core/author | "Tang W."xsd:string |
| http://purl.uniprot.org/citations/35193469 | http://purl.uniprot.org/core/author | "Zhang L."xsd:string |
| http://purl.uniprot.org/citations/35193469 | http://purl.uniprot.org/core/date | "2022"xsd:gYear |
| http://purl.uniprot.org/citations/35193469 | http://purl.uniprot.org/core/name | "Bioengineered"xsd:string |
| http://purl.uniprot.org/citations/35193469 | http://purl.uniprot.org/core/pages | "5638-5652"xsd:string |
| http://purl.uniprot.org/citations/35193469 | http://purl.uniprot.org/core/title | "AFAP1 antisense RNA 1 promotes retinoblastoma progression by sponging microRNA miR-545-3p that targets G protein subunit beta 1."xsd:string |
| http://purl.uniprot.org/citations/35193469 | http://purl.uniprot.org/core/volume | "13"xsd:string |
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