Publication: Overexpression of lncRNA IRAIN restrains the progression and Temozolomide resistance of glioma via repressing IGF-1R-PI3K-NF-κB signaling pathway
Authors
Guo, Aishun ; Fang, Guixia ; Lin, Zhenrong ; Zheng, Shuishun ; Zhuang, Zhijun ; Lin, Ruisheng ; Lin, Yanling
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Publisher
Universidad de Murcia, Departamento de Biologia Celular e Histiologia
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DOI
https://doi.org/10.14670/HH-18-425
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info:eu-repo/semantics/article
Description
Abstract
Background. 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.
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Citation
Histology and Histopathology Vol. 37, nº6 (2022)
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Este ítem está sujeto a una licencia Creative Commons. http://creativecommons.org/licenses/by-nc-nd/4.0/