miR-493 by regulating of c-Jun targets Wnt5a/PD-L1-inducing esophageal cancer cell development

Abstract Background miRNA dysregulation has been implicated in cancer development.Methods In the present study, we use cell culture and transfection, the tissue specimens, RNA isolation and RT-PCR, Western blot and so on to explore the role of miR-493 in esophageal cancer.Results Overexpression of miR-493 attenuates esophageal cancer cell proliferation, migration, and invasion in vivo and in vitro. Moreover, miR-493 downregulation is an unfavorable factor in EC and negatively correlated with Wnt5A. The existence of miR-493 is also an important attribute of metabolism. Based on mechanism analyses, we show that miR-493 inhibits the activity of c-JUN and p-PI3K/p-AKT with enhanced p21 and directly regulates Wnt5A expression and function, while, c-JUN binds the promoter region of miR-493 and suppressed the expression of miR-493, forming a negative feedback loop. Moreover, miR-493 regulates the expression of PD-L1 by c-JUN and then the sensitivity of EC cells to DDP.Conclusions the results elucidate a molecular feedback loop that involves miR-493, Wnt5A, c-JUN and PD-L1 in EC. In future, these mechanistic findings provide a useful therapeutic option for the treatment of EC.