ArticleOncogene2013
Inhibition of AHR transcription by NF1C is affected by a single-nucleotide polymorphism, and is involved in suppression of human uterine endometrial cancer.
Article in Oncogene, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.
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Who cites it
16 citing papers in PubMed, 1 synthesis or guideline pooled it, 30 citations in OpenAlex.
- Aryl hydrocarbon receptor gene transitions (c.-742C>T; c.1661G>A) and idiopathic male infertility: a case-control study with in silico and meta-analysis.Environmental science and pollution research international · 2017Pooled it
- Association of aryl hydrocarbon receptor gene polymorphisms with hashimoto's thyroiditis.Journal of endocrinological investigation · 2026Article
- Interplay between AHR genotypes, lifestyle factors and adjuvant breast cancer treatments significantly impacts clinical outcome in a population-based cohort.BJC reports · 2025Article
- Review
- The aryl hydrocarbon receptor as a tumor modulator: mechanisms to therapy.Frontiers in oncology · 2024Review
- AHR and NRF2 in Skin Homeostasis and Atopic Dermatitis.Antioxidants (Basel, Switzerland) · 2022Review
- Identification of miRNAs as diagnostic and prognostic markers in hepatocellular carcinoma.Aging · 2021Article
- Aryl Hydrocarbon Receptor and Dioxin-Related Health Hazards-Lessons from Yusho.International journal of molecular sciences · 2021Review
- Aryl Hydrocarbon Receptor in Atopic Dermatitis and Psoriasis.International journal of molecular sciences · 2019Review
- Article
- AHR gene-dioxin interactions and birthweight in the Seveso Second Generation Health Study.International journal of epidemiology · 2018Article
- Article
- Regulation of the Mechanism of TWIST1 Transcription by BHLHE40 and BHLHE41 in Cancer Cells.Molecular and cellular biology · 2015Article
- AHR promoter variant modulates its transcription and downstream effectors by allele-specific AHR-SP1 interaction functioning as a genetic marker for vitiligo.Scientific reports · 2015Article
- Analysis of the AHR gene proximal promoter GGGGC-repeat polymorphism in lung, breast, and colon cancer.Toxicology and applied pharmacology · 2015Article
- Role of AhR/ARNT system in skin homeostasis.Archives of dermatological research · 2014Review
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Involvement of the aryl hydrocarbon receptor (AHR) in carcinogenesis has been suggested in many studies. Upregulation of AHR has been reported in some cancer species, and an association between single-nucleotide polymorphisms (SNPs) of AHR and cancer risk or cancer development has also been reported. This evidence suggests the involvement of some specific SNPs in AHR transcriptional regulation in the process of carcinogenesis or cancer development, but there have been no studies to elucidate the mechanism involved. In this study, we identified the transcription factor Nuclear Factor 1-C (NF1C) as a candidate to regulate AHR transcription in a polymorphism-dependent manner. SNP rs10249788 was included in a consensus binding site for NF1C. Our results suggested that NF1C preferred the C allele to the T allele at rs10249788 for binding. Forced expression of NF1C suppressed the activity of the AHR promoter with C at rs10249788 stronger than that with T. Moreover, expression analysis of human uterine endometrial cancer (HEC) specimens showed greater upregulation of AHR and downregulation of NF1C than those of normal endometrium specimens. Sequence analysis showed HEC patients at advanced stages tended to possess T/T alleles more frequently than healthy women. We also demonstrated that NF1C suppressed proliferation, motility and invasion of HEC cells. This function was at least partially mediated by AHR. This study is the first to report that a polymorphism on the AHR regulatory region affected transcriptional regulation of the AHR gene in vitro. Because NF1C is a tumor suppressor, our new insights into AHR deregulation and its polymorphisms could reveal novel mechanisms of genetic susceptibility to cancer.
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