Long Non-Coding RNA uc003jox.1 Promotes Keloid Fibroblast Proliferation and Invasion Through Activating the PI3K/AKT Signaling Pathway

Abstract

The pathogenesis of keloids is complex and unclear, and the treatment of this condition remains challenging. The long non-coding RNA uc003jox.1 is highly expressed in keloid tissues compared with in normal skin tissues. We assessed the role of uc003jox.1 in keloid fibroblasts and its underlying mechanism, focusing on the phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT) pathway. Keloid fibroblasts were transfected with a small interfering RNA targeting uc003jox.1. Colony formation, transwell, and flow cytometry assays were conducted to evaluate the proliferation, invasion, and apoptosis of keloid fibroblasts, respectively. The interaction between uc003jox.1 and the PI3K/AKT pathway was explored by using polymerase chain reaction and western blotting. Knockdown of uc003jox.1 markedly suppressed keloid fibroblast proliferation, clone-forming activity, and invasion, as well as promoted apoptosis. Silencing of uc003jox.1 decreased the phosphorylation levels of PI3K, AKT, and mammalian target of rapamycin and increased both the mRNA and protein expression levels of phosphatase and tensin homolog. Our in vitro results suggest that the long non-coding RNA uc003jox.1 can be used as a biomarker for keloid fibroblasts and that its expression is closely related to the proliferation and invasion of keloid fibroblasts through the PI3K/AKT/mammalian target of rapamycin pathway. Thus, uc003jox.1 shows potential as a treatment target for keloids.