we examined the effect of Aurka chemical on the resistance of V617F/EpoR cells to CDDP. Curiously, Aurka inhibitor somewhat paid off the viability of V617F/EpoR cells and dramatically increased the sensitivity of V617F/EpoR cells to CDDP. Moreover, Aurka chemical increased the expression of p53 in V617F/EpoR cells. This observation well fits the effect shown in Fig. 4 and stresses that kinase activity of Aurka is critical for the regulation of p53 stability. More over, both the activation of caspase 3 and DNA fragmentation were somewhat detected in cells treated with Aurka inhibitor, and therapy with Aurka inhibitor markedly improved CDDP induced apoptosis in V617F/EpoR cells. Taken axitinib price together, it’s recommended that Aurka is important for resistance to DNA damage in cells transformed by JAK2 V617F mutant and that Aurka chemical is an efficient drug for MPNs. In the present study, we determined Aurka as an important gene induced by JAK2 V617F mutant and responded the appearance of Aurka is controlled by c Myc. Our results confirmed that the expression of c Myc is also upregulated by JAK2 V617F mutant, even though it remains to be clarified how a expression of c Myc is induced by JAK2 V617F mutant. As shown in Fig. 3A, JAK2 V617F mutant triggers resistance to CDDP treatment, and this can be strikingly abolished by the inhibition of Aurka and by knockdown of endogenous Aurka utilizing a specific chemical, suggesting that Aurka could possibly be required for the resistance Plastid to CDDP treatment induced by JAK2 V617F. Apparently, the expression amount of p53 was up regulated by knockdown of Aurka and down regulated by overexpression of Aurka. Formerly, in-vitro studies have shown that Aurka phosphorylates p53 at Ser315, leading to its ubiquitination by proteolysis and Mdm2. They also showed that silencing of Aurka results in less phosphorylation of p53 at Ser315 and improves the stability of p53. In today’s study, we observed that the expression level of p53 was increased when Aurka KD mutant was Gefitinib molecular weight expressed or endogenous Aurka was inhibited by its specific inhibitor, suggesting that kinase activity of Aurka clearly contributes to the instability of p53 downstream of JAK2 V617F mutant. When considering these results, it’s thought that Aurka KD mutant features as a negative mutant in p53 expression, although the mechanism where Aurka KD mutant checks the downregulation of p53 expression hasn’t been elucidated in this study. Furthermore, Mao et al. reported the status of p53 locus affected the big event of Aurka through the use of p53 deficient mice. These studies strongly support a substantial relationship between Aurka and p53, for that reason, in considering treatment for MPNs, not merely analyzing the pres-ence of JAK2 V617F mutation in patients but also checking the status of their p53 locus can be important in the foreseeable future.