ArticleThe Journal of investigative dermatology2011
C/EBPα expression is downregulated in human nonmelanoma skin cancers and inactivation of C/EBPα confers susceptibility to UVB-induced skin squamous cell carcinomas.
Article in The Journal of investigative dermatology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
12 citing papers in PubMed.
- The cutaneous beta human papillomavirus type 8 E6 protein induces CCL2 through the CEBPα/miR-203/p63 pathway to support an inflammatory microenvironment in epidermodysplasia verruciformis skin lesions.Frontiers in cellular and infection microbiology · 2024Article
- Evaluation of the effects of IL‑22 on the proliferation and differentiation of keratinocytes in vitro.Molecular medicine reports · 2020Article
- C/EBPβ suppresses keratinocyte autonomous type 1 IFN response and p53 to increase cell survival and susceptibility to UVB-induced skin cancer.Carcinogenesis · 2019Article
- Cross-talk of cutaneous beta human papillomaviruses and the immune system: determinants of disease penetrance.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2019Review
- Review
- Identification of C/EBPα as a novel target of the HPV8 E6 protein regulating miR-203 in human keratinocytes.PLoS pathogens · 2017Article
- Targeted BMI1 inhibition impairs tumor growth in lung adenocarcinomas with low CEBPα expression.Science translational medicine · 2016Article
- Long noncoding RNA lincRNA-p21 is the major mediator of UVB-induced and p53-dependent apoptosis in keratinocytes.Cell death & disease · 2015Article
- C/EBPα regulates CRL4(Cdt2)-mediated degradation of p21 in response to UVB-induced DNA damage to control the G1/S checkpoint.Cell cycle (Georgetown, Tex.) · 2014Article
- Article
- Control of skin cancer by the circadian rhythm.Proceedings of the National Academy of Sciences of the United States of America · 2011Article
- Treatment of nonmelanoma skin cancer with pro-differentiation agents and photodynamic therapy: Preclinical and clinical studies (Review).Photochemistry and photobiologyReview
Corrections and comments
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Authors and funding
9 authors.
Funding
Abstract
Human epidermis is routinely subjected to DNA damage induced by UVB solar radiation. Cell culture studies have revealed an unexpected role for C/EBPα (CCAAT/enhancer-binding protein-α) in the DNA damage response network, where C/EBPα is induced following UVB DNA damage, regulates the G(1) checkpoint, and diminished or ablated expression of C/EBPα results in G(1) checkpoint failure. In the current study we observed that C/EBPα is induced in normal human epidermal keratinocytes and in the epidermis of human subjects exposed to UVB radiation. The analysis of human skin precancerous and cancerous lesions (47 cases) for C/EBPα expression was conducted. Actinic keratoses, a precancerous benign skin growth and precursor to squamous cell carcinoma (SCC), expressed levels of C/EBPα similar to normal epidermis. Strikingly, all invasive SCCs no longer expressed detectable levels of C/EBPα. To determine the significance of C/EBPα in UVB-induced skin cancer, SKH-1 mice lacking epidermal C/EBPα (CKOα) were exposed to UVB. CKOα mice were highly susceptible to UVB-induced SCCs and exhibited accelerated tumor progression. CKOα mice displayed keratinocyte cell cycle checkpoint failure in vivo in response to UVB that was characterized by abnormal entry of keratinocytes into S phase. Our results demonstrate that C/EBPα is silenced in human SCC and loss of C/EBPα confers susceptibility to UVB-induced skin SCCs involving defective cell cycle arrest in response to UVB.
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Registered trials
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