BCL11A deficiency protects epidermis from UVB-induced damage through promotion of autophagy.

ABSTRACT: As a major environmental pathogenic factor for various skin diseases, UVB radiation leads to oxidative stress and biomacromolecule damage. Autophagy is a highly conserved catabolic process and serves as one of the main mechanisms to maintain cellular homeostasis. Here, by CRISPR/Cas9-mediated gene deletion, we demonstrate that the essential transcriptional repressor BCL11A is involved in autophagy regulation and participates in the UVB-induced stress response. BCL11A deficiency increases autophagosome formation and enhances the intensity of autophagy flux with or without UVB stress. Mechanistically, ACSS3, rather than autophagy-related genes, is identified as the direct target gene and transcriptionally repressed by BCL11A. Further, BCL11A deficiency reduces DNA damage and ROS to promote s

SUBMITTER: Deng X 

PROVIDER: S-EPMC12491459 | biostudies-literature | 2025 Oct

REPOSITORIES: biostudies-literature