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

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.