ArticleScientific reports2016
Deletion and low expression of NFKBIA are associated with poor prognosis in lower-grade glioma patients.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 22 citations in OpenAlex.
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- FXR activation suppresses NF-κB signaling, proliferation and migration in cervical cancer cells.Translational cancer research · 2025Article
- Article
- Identification of immune-related hub genes and construction of an immune-related gene prognostic index for low-grade glioma.Journal of cellular and molecular medicine · 2023Article
- NF-κB-Dependent and -Independent (Moonlighting) IκBα Functions in Differentiation and Cancer.Biomedicines · 2021Review
- Identification of Systems Level Molecular Signatures from Glioblastoma Multiforme Derived Extracellular Vesicles.Journal of molecular neuroscience : MN · 2021Article
- Transcriptional repression of NFKBIA triggers constitutive IKK- and proteasome-independent p65/RelA activation in senescence.The EMBO journal · 2021Article
- BioNetStat: A Tool for Biological Networks Differential Analysis.Frontiers in genetics · 2019Article
- Expression of the Circadian Clock GeneFrontiers in oncology · 2018Article
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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
Lower-grade gliomas (LGGs), which are uniformly fatal in young adults, are classified as grades II-III tumors according to their histological features. The NFκB transcription factor, a crucial player in cancer initiation and progression, is inactivated in the cytoplasm by inhibitory proteins (IκBs) that have been shown to exert tumor-suppressor activity. Therefore, using The Cancer Genome Atlas copy number alteration and RNA-Seq data from 398 patients, we evaluated the association between the expression and dosage of NFKBIA, which encodes IκBα, and the overall malignancy of LGGs. Deletion and low expression of NFKBIA were associated with enhanced tumor aggressiveness and poor prognosis in LGGs. Accordingly, the dosage and expression of NFKBIA were independent prognostic factors for 5-year survival (dosage: P = 0.016; expression: P = 0.002) and 5-year recurrence-free survival (dosage: P = 0.009; expression: P = 0.005). Moreover, gene set enrichment analyses and co-expression network analyses indicated a role for NFKBIA in the negative regulation of cell proliferation, possibly through the modulation of downstream NFκB activation. Overall, the present findings reveal the prognostic value of NFKBIA in LGGs, reinforcing the relevance of NFκB signaling in the development and progression of gliomas.
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