Previous reports from our class and the others claim that MIZ 1 positively regulates expression of other good neuroblastoma genes and genes encoding CDK inhibitors. But, it had been known that treatment of the cells with 17 DMAG induced an inferior molecular weight MIZ 1 protein as compared to that met inhibitor of MIZ 1 discovered in MIZ 1 transfected cells. In addition, effects shown in Fig. 8 were reproducible when various anti MIZ 1 antibodies were used. It should be noted that in line with the deduced amino-acid sequence of MIZ 1, its expected molecular weight is 88 kDa. To further ensure data shown in Fig. 8, we executed 2 D gel analysis using SKNAS and CHP134 treated with 17 DMAG. As shown in Fig. 9, 17 DMAG did actually produce MIZ 1 protein in these cell lines, but the drug-induced MIZ 1 protein had an inferior molecular-weight and less post translational modifications as compared to that of the cells transfected with MIZ 1. Currently, there’s been no report to show that Hsp90 inhibition contributes to down-regulation of MYC and MYCN. In this study, we have shown that Hsp90 inhibition Plastid quickly destabilizes MYCN and MYC proteins in bad neuroblastoma cells. Even though precise mechanism where Hsp90 inhibition causes destabilization of MYCN and MYC isn’t clear, our results claim that MYCN and MYC are one of the Hsp90 client proteins. Moreover, the AKT pathway is well known to support MYCN and MYC. Because treatment of neuroblastoma cells with 17 DMAG results in down regulation of AKT, one could describe the destabilization of MYC and MYCN consequently of AKT inactivation. Our data also claim that there’s yet an additional mechanism for MYC and MYCN destabilization in neuroblastoma cells having an intact p53 pathway. As described, inhibition of Hsp90 by 17 DMAG up regulates p53 expression and concomitantly destabilizes MYCN and MYC. There’s an inverse correlation Cabozantinib molecular weight between MYCN and p53 expression or MYC expression in 17 DMAG treated cell lines. This observation is consistent with our previous research, which demonstrates an increased p53 expression leads to a decreased MYCN expression in MYCN amplified neuroblastoma cells. Nevertheless, the identity of p53 targets that mediate the destabilization of MYCN and MYC in the neuroblastoma cells remains to be identified. Based on the information shown in Figs. 3 and 4, the induction of p21WAF1 is p53 independent and likely p53 dependent. It is unclear why CHP134 with the intact p53 process, fails to stimulate p21WAF1 expression in a reaction to p53 induction mediated by Hsp90 inhibition. Nevertheless, based on our knowledge, it’s more challenging to induce p21WAF1 protein expression in CHP134 by treatments as compared to other cell lines. Ergo, the p21WAF1 reaction mechanism to different environmental cues might be impaired in CHP134 cells.