ArticleCancer reports (Hoboken, N.J.)2020
Inherited variant in NFκB-1 promoter is associated with increased risk of IBD in an Algerian population and modulates SOX9 binding.
Article in Cancer reports (Hoboken, N.J.), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers, 3 of them syntheses that pooled it.
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Who cites it
7 citing papers in PubMed, 3 syntheses or guidelines pooled it, 6 citations in OpenAlex.
- NFKB1 as a key player in Tumor biology: from mechanisms to therapeutic implications.Cell biology and toxicology · 2025Pooled it
- The landscape of GWAS validation; systematic review identifying 309 validated non-coding variants across 130 human diseases.BMC medical genomics · 2022Pooled it
- Contributions of NFKB1 -94insertion/deletion ATTG polymorphism to the susceptibility of gastrointestinal cancers: A meta-analysis.Journal of cellular and molecular medicine · 2021Pooled it
- Establishment of anMethodsX · 2024Article
- Review
- NFKB1 promoter -94 insertion/deletion ATTG polymorphism (rs28362491) is associated with severity and disease progression of rheumatoid arthritis through interleukin-6 levels modulation in Egyptian patients.Clinical rheumatology · 2021Article
- Inherited variant in NFκB-1 promoter is associated with increased risk of IBD in an Algerian population and modulates SOX9 binding.Cancer reports (Hoboken, N.J.) · 2020Article
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe link between inflammation and cancer development was intensively studied in the last decade. To date, few studies explored the association between inflammatory genes and colorectal cancer (CRC) development.
aimThe present study aimed to evaluate the implication of three single nucleotide polymorphisms (SNPs), rs28362491 ins/del -94 ATTG in NFκB1, rs6920220 (G/A) in TNFAIP3, and rs419598 (C/T) in IL1RN, which play a role in inflammation regulation in CRC development. METHODS AND
resultsA case-control study was conducted on an Algerian cohort of 358 subjects (147 healthy people, 89 individuals affected by inflammatory bowel disease [IBD], and 122 CRC patients enrolled at the University Hospital Center Ben Badis of Constantine). SNPs genotyping was performed by allelic discrimination TaqMan assay. The rs28362491 ins/del heterozygous genotype in NFκB1 conferred an increased risk of IBD compared with ins/ins homozygous genotype, with an increase of twofold (OR = 2.34 [1.29-4.21]; 95% CI, 1.29-4.21, P value = 0.004). No significant association was detected for the other two variants. Dual-Luciferase Reporter Assay System performed in LoVo cells showed a significantly higher activity of the construct with ins allele of rs28362491 compared with the one harboring the del allele. Computational analysis nominated SOX9 as putative transcription factor (TF) with higher probability to bind the NFκB1 promoter at the SNP site, and we demonstrated in the in vitro assay that its overexpression modulates NFκB1 promoter activity in allele-specific manner.
conclusionWe speculate that SOX9 may modulate the NFκB1 activity by binding its promoter at the SNP site in allelic specific manner.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.