Autophagy-related LncRNA PRDM10-DT responds to UVB radiation in keratinocytes.

Ultraviolet (UV)-B radiation is a major environmental risk factor that is responsible for the development and progression of many skin disorders. Autophagy is the process of degradation and recycling of damaged cytoplasmic organelles, macromolecular aggregates, and long-lived proteins. Previously, we found that the autophagy inducer apigenin restored UVB-impaired autophagy and the cellular response by downregulating the expression of autophagy-related genes such as ATG5. To explore long noncoding RNAs (lncRNAs) involved in regulating these autophagy-related genes, in this study, we assessed the expression profiles of lncRNAs and mRNAs using a microarray in human epidermal keratinocytes (HEKs) treated with or without apigenin after UVB radiation. The expression levels of 80 selected autophagy-related genes and related lncRNAs were confirmed by quantitative real-time polymerase chain reaction (qRT‒PCR). The lncRNA PRDM10-DT was proposed to regulate IRGM based on the ceRNA and coexpression pattern and was demonstrated to be involved in autophagy regulation, proliferation and migration of HEKs by qRT‒PCR, Western blotting, colony formation and scratch wound assays, respectively. These findings suggest an autophagy-related lncRNA in response to UVB radiation that promotes the proliferation and migration of HEKs through inducing autophagy by competing microRNAs for IRGM.