Lnc056 Enhances Hair Follicle Stem Cells Proliferation by Binding Transcription Factor HNRNPUL1 to Up-Regulate TRIP6 Expression

Abstract

Hair follicles regenerate spontaneously through a cycle of anagen, catagen, and telogen, and this cycle is driven by hair follicle stem cells (HFSCs). Long non-coding RNAs (lncRNAs) have previously been implicated in hair follicle cycling processes. According to the previous lncRNA sequencing results of cashmere goats, an annotated lncRNA XR_310056.1, referred to as lnc056, was found to be differentially expressed during the hair follicle cycle. Here, the purpose of this study was to determine whether lnc056 affects the proliferation of HFSCs by regulating thyroid hormone receptor interactor 6 (TRIP6) expression in combination with the transcription factor HNRNPUL1. The expression of lnc056 in HFSCs was detected by RT-qPCR. HFSCs were then treated with lnc056 and TRIP6 overexpressing adenovirus, si-HNRNPUL1, and si-TRIP6 to detect cell viability and proliferation. In addition, we investigated the binding between lnc056 and HNRNPUL1 or HNRNPUL1 and TRIP6. Finally, the biological function of lnc056 through the HNRNPUL1/TRIP6 axis was verified by target gene recovery experiments. Lnc056 was expressed in the nuclei of HFSCs, and its overexpression promoted the proliferation of cells. Moreover, lnc056 was found to bind to the transcription factor HNRNPUL1 and promoted TRIP6 expression. Furthermore, recovery assays demonstrated that lnc056 promoted the proliferation of HFSCs via the HNRNPUL1/TRIP6 axis. In summary, the results of this study suggested that lnc056 up-regulated the expression of TRIP6 by binding to the transcription factor HNRNPUL1, thereby accelerating the proliferation of HFSCs. This study enriches the molecular mechanism of lncRNA in the hair follicle cycle and provides a potential therapeutic target for hair loss.

Keywords: TRIP6; HNRNPUL1; cashmere goat; hair follicle cycle; hair follicle stem cells; lnc056.