DDX3 overexpression resulted in E-cadherin downregulation and subsequent nuclear β-catenin translocation.140 Similarly, DDX3 inhibition by NZ51, a ring-expanded nucleoside analog that is predicted to bind to the ATP-binding site of DDX3, led to decreased proliferation, motility and invasiveness in TNBC cell lines and reduced tumor load and metastatic burden in preclinical in vivo models.141. This evidence concerns the gene DDX3X and neoplasm.