Jun is activated by TRAIL JNK dependently and promotes apoptotic cell death in malignant cells including osteosarcoma [43].Downregulation of JUN decreases the expression of matrix metalloproteinases and thereby cellular invasiveness in HT1080 cells [44]. This down-regulation may be mediated through suppression off NFKB activation [45].JUN is known to be a product of MAP2K4-activation and to mediate apoptosis by several chemotherapeutics [55].upregulation of HSPA1A and JUN expression Chemosensitivity of HT1080 to mitomycin C could significantly be increased by [34]. This evidence concerns the gene NFKB1 and osteosarcoma.