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Integrated ATAC-Seq and RNA-Seq Identify ATF3 as a Tumor Suppressor in UVB-Induced Keratinocyte Carcinogenesis
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DOI：10.3390/biology15141101.png)
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Abstract
En 中文
Chronic ultraviolet radiation B (UVB) exposure is a major environmental driver of keratinocyte carcinoma, which promotes skin tumorigenesis through epigenetic and transcriptional dysregulation. The molecular mechanism connecting chromatin remodeling, inflammatory activation and keratinocyte malignant transformation remains poorly clarified. Here, integrated ATAC-seq and RNA-seq were combined to systematically profile genome-wide chromatin accessibility and transcriptomic alterations under continuous UVB stimulation. Chromatin regions with enhanced accessibility were enriched in oncogenic genes, while differentially expressed genes primarily clustered in inflammation-related pathways. Motif analysis revealed prominent enrichment of the AP-1 transcription factor family, and ATF3 was further identified as a core regulatory molecule during malignant progression. Functional experiments verified that ATF3 suppresses chronic UVB-induced malignant behaviors. This study delineates a critical mechanism underlying chronic UVB-driven skin carcinogenesis, and provides a novel tumor suppressor and promising therapeutic target for the prevention and intervention of keratinocyte carcinoma.
Keywords:
ATAC-seq
RNA-seq
chronic UVB radiation
keratinocyte carcinogenesis
ATF3
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