Transcriptional and functional regulation of cell cycle and UV response by PPARβ in human skin epidermal cells.
Ontology highlight
ABSTRACT: Solar radiation is the main source of human exposure to UV rays, which is the major carcinogen in skin cancers by inducing DNA damage. Skin cells repair these damages by activating the DNA damage response (DDR) to safeguard genome integrity, thereby preventing skin cancers. Peroxisome proliferator-activated receptor beta (PPARβ), a druggable transcription factor, is involved in the development of UV-dependent skin cancers, although its role is not mechanistically elucidated. We showed previously that PPARβ knockout (KO) mice are less prone to UV-induced skin cancers. Here, we report that PPARβ directly regulates gene expression programs associated with cell cycle and DNA repair pathways in normal human epidermal keratinocytes (NHEK). The loss of function of PPARβ in human keratinocytes led
SUBMITTER: Nguyen TN
PROVIDER: S-EPMC11610672 | biostudies-literature | 2024 Dec
REPOSITORIES: biostudies-literature
ACCESS DATA