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Overexpression of lncRNA IRAIN restrains the progression and Temozolomide resistance of glioma via repressing IGF-1R-PI3K-NF-κB signaling pathway

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dc.contributor.authorGuo, Aishun
dc.contributor.authorFang, Guixia
dc.contributor.authorLin, Zhenrong
dc.contributor.authorZheng, Shuishun
dc.contributor.authorZhuang, Zhijun
dc.contributor.authorLin, Ruisheng
dc.contributor.authorLin, Yanling
dc.date.accessioned2023-02-20T09:49:30Z
dc.date.available2023-02-20T09:49:30Z
dc.date.issued2022
dc.description.abstractBackground. Increasing studies have found that long noncoding RNAs (lncRNAs) contribute to regulating tumor progression. This study explores the expression characteristics, effects, and related mechanisms of lncRNA IGF1R antisense imprinted nonprotein coding RNA (IRAIN) in glioma. Methods. Quantitative real-time PCR (qRT-PCR) was implemented to testify the IRAIN profile in glioma tissues and paracancerous tissues, and the link between the IRAIN level and the clinicopathological indicators of glioma was analyzed. IRAIN overexpression and knockdown cell models were constructed in glioma cells. Cell proliferation was verified by the colony formation experiment, while flow cytometry was implemented to monitor apoptosis. Transwell assay was performed to examine cell invasion and migration. Western blot (WB) was adopted to compare the profiles of the apoptosis-related proteins (Bax, Bcl2, and Caspase3) and IGF-1R-PI3K-NF-κB pathway. Results. IRAIN was down-regulated in glioma tissues (compared with adjacent normal tissues), and the low IRAIN expression was significantly linked with the larger tumor volume and higher pathological stages. Functionally, overexpressing IRAIN abated glioma cell proliferation, invasion, and migration, promoted apoptosis, and attenuated IGF-1R-PI3K-NF-κB expression and temozolomide (TMZ) resistance, which was also confirmed in the xenograft tumor experiment. The WB result showed that overexpressing IRAIN inactivated the IGF-1R-PI3K-NF-κB pathway. Additionally, the IGF-1R knockdown model was established in U251 cells. Si-IGF-1R induced cell proliferation inhibition, promoted cell death, and reduced cell migration and TMZ resistance, whereas SiIGF-1R+IRAIN group showed no additional effects on glioma cells compared with the Si-IGF-1R group. Conclusion. IRAIN repressed glioma development and TMZ resistance by inactivating the IGF-1R-PI3KNF-κB axis.es
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dc.format.extent12es
dc.identifier.citationHistology and Histopathology Vol. 37, nº6 (2022)
dc.identifier.doihttps://doi.org/10.14670/HH-18-425
dc.identifier.issn0213-3911
dc.identifier.issn1699-5848
dc.identifier.urihttp://hdl.handle.net/10201/128585
dc.languageenges
dc.publisherUniversidad de Murcia, Departamento de Biologia Celular e Histiologiaes
dc.relationSin financiación externa a la Universidades
dc.rightsinfo:eu-repo/semantics/openAccesses
dc.rightsAttribution-NonCommercial-NoDerivatives 4.0 Internacional*
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/*
dc.subjectGliomaes
dc.subjectIRAINes
dc.subjectSignaling pathwayes
dc.subjectTemozolomidees
dc.subjectResistancees
dc.subject.otherCDU::6 - Ciencias aplicadas::61 - Medicina::616 - Patología. Medicina clínica. Oncologíaes
dc.titleOverexpression of lncRNA IRAIN restrains the progression and Temozolomide resistance of glioma via repressing IGF-1R-PI3K-NF-κB signaling pathwayes
dc.typeinfo:eu-repo/semantics/articlees
dspace.entity.typePublicationes
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Histology and histopathology Vol.37, nº6 (2022)