RDF/XMLNTriplesTurtleShow queryShare
SubjectPredicateObject
http://purl.uniprot.org/citations/34288816http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/34288816http://www.w3.org/2000/01/rdf-schema#comment"Ovarian cancer (OC) is one of the most common malignancies with high incidence and mortality and the eighth most common cancer-associated mortality in women worldwide. Aberrant expression of the GINS complex subunit 2 (GINS2) gene and miR-502-5p has been associated with cancer progression. This study aims to investigate the specific molecular mechanism of the miR-502-5p-GINS2 axis in OC. GINS2 and miR-502-5p expression in OC tissues and cell lines was measured using RT-qPCR. Next, we investigated the interaction between miR-502-5p and GINS2 using a luciferase assay. The role of the miR-502-5p-GINS2 axis was detected by assessing cell proliferation, migration, and apoptosis levels, such as caspase-3 activity and caspase-3 protein expression, in the OC cell lines CaOV3 and SKOV3, respectively. MiR-502-5p expression was decreased, and GINS2 expression was dramatically elevated in OC tissues and cells. Upregulation of miR-502-5p expression repressed cellular proliferation and migration levels but increased the cellular apoptosis level. GINS2 overexpression enhanced the proliferation and migration levels but hampered OC cell apoptosis. Moreover, miR-502-5p inhibited GINS2 expression and suppressed OC tumorigenesis. miR-502-5p targeting GINS2 suppressed OC progression by inhibiting cell growth and promoting cell apoptosis. Hence, we provide a comprehensive understanding of OC involving both miR-502-5p and GINS2, which might be effective therapeutic targets for OC patients."xsd:string
http://purl.uniprot.org/citations/34288816http://purl.org/dc/terms/identifier"doi:10.1080/21655979.2021.1946347"xsd:string
http://purl.uniprot.org/citations/34288816http://purl.uniprot.org/core/author"Cheng Y."xsd:string
http://purl.uniprot.org/citations/34288816http://purl.uniprot.org/core/author"Liu Y."xsd:string
http://purl.uniprot.org/citations/34288816http://purl.uniprot.org/core/author"Liu H."xsd:string
http://purl.uniprot.org/citations/34288816http://purl.uniprot.org/core/author"Yang J."xsd:string
http://purl.uniprot.org/citations/34288816http://purl.uniprot.org/core/author"Zhan L."xsd:string
http://purl.uniprot.org/citations/34288816http://purl.uniprot.org/core/date"2021"xsd:gYear
http://purl.uniprot.org/citations/34288816http://purl.uniprot.org/core/name"Bioengineered"xsd:string
http://purl.uniprot.org/citations/34288816http://purl.uniprot.org/core/pages"3336-3347"xsd:string
http://purl.uniprot.org/citations/34288816http://purl.uniprot.org/core/title"MicroRNA miR-502-5p inhibits ovarian cancer genesis by downregulation of GINS complex subunit 2."xsd:string
http://purl.uniprot.org/citations/34288816http://purl.uniprot.org/core/volume"12"xsd:string
http://purl.uniprot.org/citations/34288816http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/34288816
http://purl.uniprot.org/citations/34288816http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/34288816
http://purl.uniprot.org/uniprot/#_Q53G08-mappedCitation-34288816http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/34288816
http://purl.uniprot.org/uniprot/#_Q9Y248-mappedCitation-34288816http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/34288816
http://purl.uniprot.org/uniprot/Q53G08http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/34288816
http://purl.uniprot.org/uniprot/Q9Y248http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/34288816