Other than non-melanoma skin cancer, prostate cancer has the most common incidence of this disease in the United States. 14% of newly diagnosed cancer cases are due to prostate cancer. In addition, prostate cancer is the second leading cancer among African Americans. The uses of chemotherapy drugs have caused a major decrease in the mortality rate of cancer patients. Prostate cancer patients usually have a typical treatment of chemotherapy drugs. Some chemotherapy drugs have microtubule binding agents, which bind to the alpha tubulin on the microtubule. This investigation studies how the use of taxol, nocodazole, and HTI-286 cause the inhibition of cell division through the use of the binding sites on the tubulin of the microtubule. Specific observations were tested through the treatment of DU-145 prostate cancer cells with taxol, nocodazole, and HTI-286. In order to fully understand the mechanism of the drugs on DU-145 cells, the abilities of these chemotherapy drugs were tested through immunofluorescence and polymerization assays. The results observed showed that polymerization of tubulin caused by taxol enabled the cells to have striated and narrow tubulin effect. Both taxol and HTI-286 were depolymerized and nocodazole was found to have clusters of compacted tubulin. Even though the binding sites are different (alpha-tubulin for taxol and nocodazole) and beta-tubulin for HTI-286, all three drugs arrested cell growth and division of cancer cells. The results collectively pinpoint that these chemotherapy drugs (singly or in combination) should be considered for further investigations as possible treatments for prostate cancer.