we examined the effect of Aurka inhibitor 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. In-addition, Aurka chemical enhanced the expression of p53 in V617F/EpoR cells. This statement well matches the effect shown in Fig. 4 and emphasizes that kinase activity of Aurka is critical for the regulation of p53 stability. Moreover, the activation of caspase 3 and DNA fragmentation were slightly found in cells treated with Aurka inhibitor, and treatment with Aurka inhibitor considerably improved CDDP induced apoptosis in cells. Taken AZD5363 together, it’s recommended that Aurka is important for resistance to DNA damage in cells transformed by JAK2 V617F mutant and that Aurka inhibitor is an effective drug for MPNs. In the present research, we identified as an crucial gene induced by JAK2 V617F mutant and responded the expression of Aurka is controlled by c Myc Aurka. Our results confirmed that the expression of c Myc is also upregulated by JAK2 V617F mutant, though it remains to be clarified how the expression of c Myc is caused by JAK2 V617F mutant. As shown in Fig. 3A, JAK2 V617F mutant causes resistance to CDDP treatment, and this is specifically removed by the inhibition of Aurka and by knock-down of endogenous Aurka using a specific chemical, suggesting that Aurka might be needed for the resistance Infectious causes of cancer to CDDP treatment induced by JAK2 V617F. Curiously, the expression degree 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, resulting in its ubiquitination by proteolysis and Mdm2. In addition they showed that silencing of Aurka results in phosphorylation of p53 at Ser315 and increases the stability of p53. In today’s study, we observed that the expression level of p53 was increased when Aurka KD mutant was Cabozantinib structure expressed or endogenous Aurka was restricted by its specific inhibitor, indicating that kinase activity of Aurka strongly contributes to the uncertainty of p53 downstream of JAK2 V617F mutant. When contemplating these results, it is believed that Aurka KD mutant functions as a negative mutant in p53 expression, even though the system through which Aurka KD mutant stops the downregulation of p53 expression hasn’t been elucidated in this study. More over, Mao et al. Noted the status of p53 locus influenced the event of Aurka through the use of p53 deficient mice. These studies strongly support a substantial relationship between Aurka and p53, consequently, in considering treatment for MPNs, not just examining the presence of JAK2 V617F mutation in patients but also examining the position of their p53 locus can be important later on.