UVB-induced decrease of p16/CDKN2A expression in skin cancer patients
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Updated: Oct 5, 2026

Spatial and Temporal Control of Murine Melanoma Initiation from Mutant Melanocyte Stem Cells
Published on: June 7, 2019
1Department of Dermatology, University of Munich, Germany. ulrike.leiter@medizin.uni-ulm.de
Abstract:
The lack of p16 expression has been shown in cultured melanoma cells, however contradictory evidence for p16 expression in melanoma tissues exist. Ultraviolet (UV) C and UVB have been shown to affect p16 expression, which impairs cell cycle regulation in vitro and in vivo. In this study, p16/CDKN2A gene expression was determined by reverse transcription polymerase chain reaction in seven skin cancer patients, in one dysplastic nevus patient and in seven healthy individuals, prior to UVB exposure and at various times after application of one minimal erythema dose (MED). Five of the seven skin cancer patients showed a down-regulation of p16/CDKN2A expression after UVB exposure, while controls remained unaltered. The UVB-induced decline of p16/CDKN2A in skin cancer patients might offer new insights into photocarcinogenesis. The putative sequence of events could start with a down-regulation of p16/CDKN2A expression, which would lead to impaired cell cycle regulation. Altered expression patterns of p16/CDKN2A following UVB exposure could be of value for identifying people with an increased risk of UV-induced skin cancer.
Insights
UVB exposure down-regulates p16/CDKN2A gene expression in skin cancer patients, unlike healthy individuals. This decline in p16/CDKN2A may impair cell cycle regulation, offering insights into UV-induced skin cancer development.
Area of Science:
- Dermatology
- Molecular Biology
- Cancer Research
Background:
- p16 expression in melanoma tissues is contradictory.
- Ultraviolet (UV) radiation, including UVB, impacts p16 expression and cell cycle regulation.
- p16/CDKN2A is a key tumor suppressor gene involved in cell cycle control.
Purpose of the Study:
- To investigate the effect of UVB exposure on p16/CDKN2A gene expression in skin cancer patients and healthy individuals.
- To explore the role of p16/CDKN2A down-regulation in UV-induced skin carcinogenesis.
Main Methods:
- Reverse transcription polymerase chain reaction (RT-PCR) was used to quantify p16/CDKN2A gene expression.
- Participants included skin cancer patients, a dysplastic nevus patient, and healthy controls.
- Samples were analyzed before and after controlled UVB exposure (one minimal erythema dose).
Main Results:
- Five out of seven skin cancer patients exhibited down-regulation of p16/CDKN2A expression post-UVB exposure.
- Healthy individuals and the dysplastic nevus patient showed no significant alteration in p16/CDKN2A expression after UVB.
- UVB-induced decline in p16/CDKN2A was observed specifically in skin cancer patients.
Conclusions:
- UVB-induced down-regulation of p16/CDKN2A in skin cancer patients suggests a potential mechanism in photocarcinogenesis.
- Impaired cell cycle regulation due to decreased p16/CDKN2A may contribute to skin cancer development.
- Altered p16/CDKN2A expression patterns after UVB exposure could serve as a biomarker for identifying individuals at higher risk of UV-induced skin cancer.
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