Further mechanistic studies demonstrated that TChal could bind and degrade chromosome region maintenance 1 (CRM1), a nuclear export receptor involved in the active transport of tumor suppressors, and increase heat-shock protein 40 (HSP40) expression in U2OS osteosarcoma cells; the interaction of HSP40 with MDM2 blocked MDM2-mediated ubiquitination of p53, leading to the enhanced stability and activation of p53 [128,130]. This evidence concerns the gene TP53 and osteosarcoma.