ArticleMedical science monitor : international medical journal of experimental and clinical research2020
Silencing of Long Non-Coding RNA (LncRNA) Non-Coding RNA Activated by DNA Damage (NORAD) Inhibits Proliferation, Invasion, Migration, and Promotes Apoptosis of Glioma Cells via Downregulating the Expression of AKR1B1.
Article in Medical science monitor : international medical journal of experimental and clinical research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 9 citations in OpenAlex.
- Resveratrol inhibits the progression of oral squamouscell carcinoma through Norad/Igf2bp2/Pdk1 pathway and remodeling glucose metabolism reprogramming.Discover oncology · 2025Article
- Aldo-keto reductases: Role in cancer development and theranostics.Oncology research · 2024Review
- Article
- LncRNAJournal of gastrointestinal oncology · 2022Article
- A Potential Prognostic Biomarker for Glioma: Aldo-Keto Reductase Family 1 Member B1.Computational intelligence and neuroscience · 2022Article
- So alike yet so different. Differential expression of the long non-coding RNAs NORAD and HCG11 in breast cancer subtypes.Genetics and molecular biology · 2021Article
- Non-coding RNA Activated by DNA Damage: Review of Its Roles in the Carcinogenesis.Frontiers in cell and developmental biology · 2021Review
- Genome-wide profiling of lncRNAs in pediatric intracranial ependymomas identifiesNeuro-oncology advancesArticle
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND We aimed to investigate the functions of long non-coding RNA (lncRNA) non-coding RNA activated by DNA damage (NORAD) in glioma and identify the potential mechanisms. MATERIAL AND METHODS The expression of NORAD and AKR1B1 in human glioma cell lines were examined using reverse transcription-quantitative polymerase chain reaction (RT-qPCR). Then, cell proliferation, invasion, and migration were tested by Cell Counting Kit-8 (CCK-8), colony formation assay, Transwell, and scratch wound healing assay after NORAD silencing. Meanwhile, western blotting was utilized to measure the expression of migration-related proteins. Apoptosis of glioma cells was detected using flow cytometry and apoptosis-related proteins expression was determined. Moreover, the correlation between NORAD and AKR1B1 was verified by RNA-binding protein immunoprecipitation (RIP assay). After co-transfection with AKR1B1 overexpressed plasmid and NORAD siRNA, cell proliferation, invasion, migration, and apoptosis were examined again. Furthermore, the expression of proteins in extracellular signal-regulated kinase (ERK) signaling was tested using western blotting. RESULTS The results revealed that NORAD and AKR1B1 were highly expressed in glioma cells. NORAD silencing inhibited proliferation, invasion and migration but promoted apoptosis of glioma cells, accompanied by the expression changes of migration- and apoptosis-related proteins. However, after co-transfection with AKR1B1 pcDNA3.1 in NORAD silencing cells, the effects of NORAD silencing on proliferation, invasion, migration, and apoptosis were attenuated. Consistently, the expression of phosphorylated ERK (p-ERK) was decreased after NORAD silencing, which were reversed following AKR1B1 overexpression. CONCLUSIONS These findings demonstrated that NORAD silencing suppressed proliferation, invasion, and migration and boosted apoptosis of glioma cells via downregulating the AKR1B1 expression, which may provide a potential therapeutic target for glioma treatment.
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