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http://purl.uniprot.org/citations/31750728http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/31750728http://www.w3.org/2000/01/rdf-schema#comment"Background: Glioma is a common malignant tumor. The purpose of this study was to investigate the effect and molecular mechanism of long noncoding RNA (lncRNA) NCK1-AS1 on the drug resistance of temozolomide (TMZ) in glioma cells. Methods: The fresh and recurrent glioma tissues and peritumoral brain edema (PTBE) were collected from the same patient. U251 and A172 cells were treated with TMZ to screen TMZ-resistant cells. The expression levels of NCK1-AS1, miR-137, or TRIM24 were detected by quantitative real-time polymerase chain reaction (qRT-PCR), Western blotting, in situ hybridization (ISH), or RNA pull-down assay. Cell viability was measured by 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazoliumbromide (MTT) assay. In addition, the relationship between NCK1-AS1 and miR-137 or TRIM24 and miR-137 was confirmed by dual luciferase activity assay. Results: NCK1-AS1 expression was increased in regular and recurrent glioma tissues and TMZ-resistant cells. Cell viability was increased in TMZ-resistant cells, and the IC50 of TMZ also increased in TMZ resistant cells. However, knockdown of NCK1-AS1 inhibited these increases. Moreover, suppression of NCK1-AS1 increased miR-137 expression, whereas overexpression of miR-137 decreased TRIM24 expression. Then, expression of miR-137 alleviated the NCK1-AS1 overexpression-induced increased expression of TRIM24. In addition, the decreases of cell viability and IC50 induced by NCK1-AS1 knockdown were reversed after adding TRIM24 in U251/TMZ and A172/TMZ cells. Conclusion: NCK1-AS1 could increase drug resistance of glioma cells to TMZ by modulating miR-137/TRIM24 pathway."xsd:string
http://purl.uniprot.org/citations/31750728http://purl.org/dc/terms/identifier"doi:10.1089/cbr.2019.3054"xsd:string
http://purl.uniprot.org/citations/31750728http://purl.uniprot.org/core/author"Chen M."xsd:string
http://purl.uniprot.org/citations/31750728http://purl.uniprot.org/core/author"Cheng Y."xsd:string
http://purl.uniprot.org/citations/31750728http://purl.uniprot.org/core/author"Zhao H."xsd:string
http://purl.uniprot.org/citations/31750728http://purl.uniprot.org/core/author"Wang F."xsd:string
http://purl.uniprot.org/citations/31750728http://purl.uniprot.org/core/author"Yang L."xsd:string
http://purl.uniprot.org/citations/31750728http://purl.uniprot.org/core/author"Yuan Z."xsd:string
http://purl.uniprot.org/citations/31750728http://purl.uniprot.org/core/date"2020"xsd:gYear
http://purl.uniprot.org/citations/31750728http://purl.uniprot.org/core/name"Cancer Biother Radiopharm"xsd:string
http://purl.uniprot.org/citations/31750728http://purl.uniprot.org/core/pages"101-108"xsd:string
http://purl.uniprot.org/citations/31750728http://purl.uniprot.org/core/title"NCK1-AS1 Increases Drug Resistance of Glioma Cells to Temozolomide by Modulating miR-137/TRIM24."xsd:string
http://purl.uniprot.org/citations/31750728http://purl.uniprot.org/core/volume"35"xsd:string
http://purl.uniprot.org/citations/31750728http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/31750728
http://purl.uniprot.org/citations/31750728http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/31750728
http://purl.uniprot.org/uniprot/#_B4DYZ9-mappedCitation-31750728http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/31750728
http://purl.uniprot.org/uniprot/#_O15164-mappedCitation-31750728http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/31750728
http://purl.uniprot.org/uniprot/O15164http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/31750728
http://purl.uniprot.org/uniprot/B4DYZ9http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/31750728