| http://purl.uniprot.org/citations/34009012 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/34009012 | http://www.w3.org/2000/01/rdf-schema#comment | "Background: Poly ADP-ribose polymerase 1 (PARP1) has been discovered to be implicated in ovarian cancer (OC), but its interaction with microRNA (miR)-519a-3p remained poorly understood. This study aimed to uncover their roles and interactions in OC. Materials and Methods: Clinical tissue from OC patients and adjacent normal tissue were collected, and the survival rates of OC patients with high or low PARP1 expression were analyzed by Kaplan-Meier curve. After transfection, OC cell viability, migration, and tube formation were detected with cell counting kit-8 (CCK-8) assay, scratch assay, and tube formation assay, respectively. The target gene of miR-519a-3p and potential binding sites between them were predicted with TargetScan and confirmed using a dual-luciferase reporter assay. Relative expressions of miR-519a-3p, PARP1, E-cadherin, N-cadherin, SNAIL, vascular endothelial growth factor (VEGF), and p53 were measured by quantitative real-time polymerase chain reaction and Western blot as needed. Results: PARP1 expression was upregulated in OC, which was related to poor prognosis of OC patients. Silencing PARP1 decreased PARP1 expression and suppressed viability, migration, invasion, and tube formation in OC cells, while overexpressed PARP1 did the opposite. PARP1 was the target gene of miR-519a-3p, and it reversed the effects of miR-519a-3p on the migration, invasion, and tube formation of OC cells by upregulating the expressions of PAR, PARP1, N-cadherin, SNAIL, and VEGF and downregulating those of E-cadherin and p53. Conclusion: PARP1, a target gene of miR-519a-3p, promoted the migration, invasion, and tube formation of OC cells, providing a possible therapeutic target for treatment of OC patients."xsd:string |
| http://purl.uniprot.org/citations/34009012 | http://purl.org/dc/terms/identifier | "doi:10.1089/cbr.2020.4394"xsd:string |
| http://purl.uniprot.org/citations/34009012 | http://purl.uniprot.org/core/author | "Chang H."xsd:string |
| http://purl.uniprot.org/citations/34009012 | http://purl.uniprot.org/core/author | "Li B."xsd:string |
| http://purl.uniprot.org/citations/34009012 | http://purl.uniprot.org/core/author | "Zhang X."xsd:string |
| http://purl.uniprot.org/citations/34009012 | http://purl.uniprot.org/core/author | "Meng X."xsd:string |
| http://purl.uniprot.org/citations/34009012 | http://purl.uniprot.org/core/date | "2022"xsd:gYear |
| http://purl.uniprot.org/citations/34009012 | http://purl.uniprot.org/core/name | "Cancer Biother Radiopharm"xsd:string |
| http://purl.uniprot.org/citations/34009012 | http://purl.uniprot.org/core/pages | "824-836"xsd:string |
| http://purl.uniprot.org/citations/34009012 | http://purl.uniprot.org/core/title | "PARP1 Is Targeted by miR-519a-3p and Promotes the Migration, Invasion, and Tube Formation of Ovarian Cancer Cells."xsd:string |
| http://purl.uniprot.org/citations/34009012 | http://purl.uniprot.org/core/volume | "37"xsd:string |
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