ArticlePloS one2012
Loss of hairless confers susceptibility to UVB-induced tumorigenesis via disruption of NF-kappaB signaling.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 23 citations in OpenAlex.
- The dynamics of mutational selection in cutaneous squamous carcinogenesis.Communications biology · 2026Article
- Macrophage migration inhibitory factor (MIF) and its homolog D-dopachrome tautomerase (D-DT) are significant promotors of UVB- but not chemically induced non-melanoma skin cancer.Scientific reports · 2023Article
- Topical GZ21T Inhibits the Growth of Actinic Keratoses in a UVB-Induced Model of Skin Carcinogenesis.JID innovations : skin science from molecules to population health · 2023Article
- The Histone Demethylase HR Suppresses Breast Cancer Development through Enhanced CELF2 Tumor Suppressor Activity.Cancers · 2022Article
- Role of hair follicles in the pathogenesis of arsenical-induced cutaneous damage.Annals of the New York Academy of Sciences · 2022Article
- Control of Breast Cancer Pathogenesis by Histone Methylation and the Hairless Histone Demethylase.Endocrinology · 2021Review
- Plasma Treatment Limits Cutaneous Squamous Cell Carcinoma Development In Vitro and In Vivo.Cancers · 2020Article
- Identification of master regulator genes of UV response and their implications for skin carcinogenesis.Carcinogenesis · 2019Article
- Comparison of the acute ultraviolet photoresponse in congenic albino hairless C57BL/6J mice relative to outbred SKH1 hairless mice.Experimental dermatology · 2016Article
- Vitis vinifera seeds extract for the modulation of cytosolic factors BAX-α and NF-kB involved in UVB-induced oxidative stress and apoptosis of human skin cells.Clujul medical (1957) · 2016Article
- Increased Susceptibility to Skin Carcinogenesis Associated with a Spontaneous Mouse Mutation in the Palmitoyl Transferase Zdhhc13 Gene.The Journal of investigative dermatology · 2015Article
- Shh and p50/Bcl3 signaling crosstalk drives pathogenesis of BCCs in Gorlin syndrome.Oncotarget · 2015Article
- Keratin-6 driven ODC expression to hair follicle keratinocytes enhances stemness and tumorigenesis by negatively regulating Notch.Biochemical and biophysical research communications · 2014Article
- Hair follicle disruption facilitates pathogenesis to UVB-induced cutaneous inflammation and basal cell carcinoma development in Ptch(+/-) mice.The American journal of pathology · 2014Article
- Inhibition of p38 MAPK signaling augments skin tumorigenesis via NOX2 driven ROS generation.PloS one · 2014Article
- Hairless and the polyamine putrescine form a negative regulatory loop in the epidermis.Experimental dermatology · 2013Article
- Nitric oxide-releasing sulindac is a novel skin cancer chemopreventive agent for UVB-induced photocarcinogenesis.Toxicology and applied pharmacology · 2013Article
- A role for NF-κB activity in skin hyperplasia and the development of keratoacanthomata in mice.PloS one · 2013Article
- Transcriptome sequencing of neonatal thymic epithelial cells.Scientific reports · 2013Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
In order to model squamous cell carcinoma development in vivo, researchers have long preferred hairless mouse models such as SKH-1 mice that have traditionally been classified as 'wild-type' mice irrespective of the genetic factors underlying their hairless phenotype. The work presented here shows that mutations in the Hairless (Hr) gene not only result in the hairless phenotype of the SKH-1 and Hr(-/-) mouse lines but also cause aberrant activation of NFκB and its downstream effectors. We show that in the epidermis, Hr is an early UVB response gene that regulates NFκB activation and thereby controls cellular responses to irradiation. Therefore, when Hr expression is decreased in Hr mutant animals there is a corresponding increase in NFκB activity that is augmented by UVB irradiation. This constitutive activation of NFκB in the Hr mutant epidermis leads to the stimulation a large variety of downstream effectors including the cell cycle regulators cyclin D1 and cyclin E, the anti-apoptosis protein Bcl-2, and the pro-inflammatory protein Cox-2. Therefore, Hr loss results in a state of uncontrolled epidermal proliferation that promotes tumor development, and Hr mutant mice should no longer be considered merely hairless 'wild-type' mice. Instead, Hr is a crucial UVB response gene and its loss creates a permissive environment that potentiates increased tumorigenesis.
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Registered trials
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.