HRAS and glioblastoma: Consequently, H-Ras may be a potential target against Gal-1-induced HCC progression.25 Moreover, Gal-1 activates NF-κB in kidney cancer, inducing CXCR4 expression.26 The SDF-1/CXCR4 axis can trigger EMT in glioblastoma,27 meaning that CXCR4 could be another downstream target that mediates Gal-1-induced HCC progression; however, our results indicate that forced expression of Gal-1 in HCC cells is accompanied by an upregulation of αvβ3-integrin mRNAs and proteins.