Early time course studies showed that the result of the prescription drugs on p53 expression varied among the cell lines analyzed. An enhancement of p53 expression was most evident in IMR5, where p53 expression was elevated after 6 h of the drug treatment. There is no apparent impact on p53 expression in SY5Y and CHP134 up to 9 h of the drug therapy. Cabozantinib Tie2 kinase inhibitor WAF1 As identified, Hsp90 inhibition increased p53 expression within the neuroblastoma cells. We therefore examined if 17 DMAG therapy up regulated the expression of p21WAF1, a known target of p53. As shown in Fig. 4, Hsp90 inhibition by 17 DMAG resulted in a upregulation of p21WAF1 expression in SY5Y and IMR5 cells, but not in CHP134. SKNAS with TP53 mutations showed little induction of p21WAF1 expression upon the drug therapy. AKT is a known customer protein of Hsp90, and hence inhibition of Hsp90 results in deterioration of AKT. Moreover, the AKT pathway is famous to secure Urogenital pelvic malignancy MYC and MYCN. We ergo examined the effect of Hsp90 inhibition by 17 DMAG on AKT balance in the neuroblastoma cells as a get a handle on, and to compare for the MYCN and MYC destabilization described in Fig. 2A. As shown in Fig. 5A, 17 DMAG treatment of the neuroblastoma cells triggered a low AKT expression. Kinetics of AKT destabilization resembled to those of MYCN and MYC down-regulation in the neuroblastoma cell lines analyzed. Additionally, Hsp90 inhibition by 17 DMAG treatments didn’t change the subcellular localization of MYCN, AKT and MYC in CHP134 and SKNAS cells. Subcellular localization of these proteins inside the drug addressed SY5Y and IMR5 was not analyzed. 1To handle a possible role of Hsp90 inhibition in interfering with mitosis, we examined the appearance of acetylated tubulin in the 17 DMAG treated neuroblastoma cells. As shown in Fig. 6, there is a heightened expression of acetylated tubulin in the drug treated cells, indicating E2 conjugating that tubulin deacetylase levels were down-regulated by Hsp90 inhibition. The truth is, expression levels of the tubulin deacetylase, HDAC6, were markedly suppressed in these cells. Positive neuroblastoma genes are regarded as growth suppressive. We asked whether Hsp90 inhibition up licensed positive neuroblastoma genes in SKNAS as an alternative procedure to p53 pathways in suppressing growth of those cells, because SKNAS can be a TP53 mutated cell line. As shown in Fig. 7, therapy of SKNAS cells with 17 DMAG led to a heightened expression of development suppressive genes as well as positive neuroblastoma genes. So far, MIZ 1 will be the only known beneficial neuroblastoma gene to encode a transcription factor. We thus investigated if MIZ 1 protein expression was also upregulated in the 17 DMAG treated cell lines. As shown in Fig. 8, MIZ 1 protein was detected in the four cell lines handled with 17 DMAG.