Downregulating the expression of Aurora kinase An or B results in inhibition of melanoma cell proliferation. In addition, immunoblot examination of WM1158 MGP melanoma cells incubated in the presence of nocodazole for 20 hours, followed by addition of 10 uM of the Aurora kinase small molecule compound for 5, 10, or 60 minutes, demonstrated that Ser10 on histone H3 was no more phosphorylated at 60 minutes post-treatment. Immunofluorescence imaging of WM1158 MGP cancer cells that had been treated with the Aurora kinase E3 ubiquitin ligase inhibitor inhibitor for 2 hours and then were probed with an antibody to Aurora kinase A pT288 as well as an antibody to tubulin, or that had been incubated in the presence of nocodazole and afterwards were treated for 2 hours with the inhibitor and then stained with an antibody to pHisH3 as well as an tubulin antibody, revealed significant perturbation of the microfilament structure when compared to cells that weren’t treated with the inhibitor. More over, immunofluorescence imaging of nocodazole treated WM1158 MGP melanoma cells that were treated for 2 hours with the Aurora kinase inhibitor and then probed with antibody to CREST to mark kinetochores, Aurora kinase A, Aurora kinase B, in addition to or y tubulin demonstrated disruption of the spindle checkpoint compared to WM1158 MGP melanoma cells that had not been treated Organism with the little molecule agent. Blocking the big event of Aurora kinase An and B checks melanoma cell proliferation and triggers melanoma cell cycle dysregulation and apoptosis. To decide whether, as in the case of downregulating the expression of the Aurora kinases by means of RNA interference, interfering with their characteristics would lead to inhibition of melanoma cell growth, we treated MGP melanoma cells with the Aurora kinase inhibitor for approximately 5 days. As shown in Figure 5A, starting as soon as 24 hours post-treatment, the proliferation of the ubiquitin-conjugating cancer cells was markedly inhibited and to a notably greater degree than in the last experimental environment where we had suppressed via siRNAs and the expression of Aurora kinase An and also of Aurora kinase B. To evaluate whether, along with with blocking the proliferation of cancer cells, therapy with the Aurora kinase inhibitor also interfered with the cells development through the cell cycle, we attacked experiments that involved propidium iodide in addition to annexin V/propidium iodide based flow cytometry. WM1158 MGP melanoma cells that were treated for 72 hours with 10 uM of the Aurora kinase inhibitor and then fixed and labeled with propidium iodide revealed a significant accumulation of the cells in sub G0/G1, and flow cytometric analysis of annexin V/propidium iodide labeled melanoma cells that have been treated for 24 or 48 hours with the small molecule inhibitor documented that substantially more cells were arrested in the early rather than in the late-stage of apoptosis.