The current literature has shown that inhibition SU11274 PKI-SU11274 of KSP mitosis st rt And leads to cell death. Inhibition of KSP affects the formation of the bipolar spindle for the separation and purification of chromosomes w During mitosis. This chromosome abnormality leads to programmed cell death in mitotic cells. Here we have shown that SB715992 cell death induced apoptosis significantly PC 3 prostate cancer cells, suggesting that SB715992 could inhibit the formation of the bipolar spindle w During cell division, entered Ing cellular death Ren apoptosis PC 3 The gene expression profiles of SB715992 ver Changed, we found that the cellular Ren and molecular responses to SB715992 treatment are complex and are likely to be induced by a variety of regulatory pathways.
SB715992 regulates the expression of genes important for cell growth on, embroidered apoptosis, transcription, translation, and cell signaling. These rules k Can for inhibiting the progression of prostate cancer. It is well known that cyclin protein to cyclin dependent-Dependent kinases and CDK inhibitors and embroidered l connected to the process of the cell cycle. CDK inhibitors such as p27KIP1, p15 and p57Kip2 have been shown to arrest the cell cycle and inhibit the growth of cancer cells. The gene expression profiles, we found that SB715992 the expression of several cyclin-dependent-Dependent kinase inhibitors, including normal p27KIP1, p15 and p57Kip2 erh Ht, indicating a positive changes Amend the F promotion Inhibitors of cyclin-dependent -dependent kinases, which ultimately lead to cell cycle arrest.
Au Addition went SB715992 the expression of genes such as the growth factor and fibroblast growth factor and epidermal these genes are important molecules for the survival and proliferation. Therefore, the expression of these genes fall k Nnten negatively regulate cell cycle, cell proliferation, angiogenesis, motility t, metastasis, and cell signaling. Another objective of this study was to determine whether genistein, an isoflavone potentiate natural, k Nnte the effect of SB715992 on human prostate cancer cells. Previously been shown to genistein, the nucleic Re transcription factor NF B ? and inhibit Akt signaling pathways in cancer cells, leading to apoptosis. Genistein has also been shown to angiogenesis and inhibits topoisomerase I and II.
Our study showed that genistein increased Hte the growth inhibitory effect of SB715592 on PC 3 cells. Moreover, we have also found that genistein could induced improve the induction of apoptosis in cells by PC 3 SB715992, suggesting that genistein may be useful clinically, when combined with SB715992. Therefore, we believe that SB715992 could be used as a new therapy for prostate cancer and treatment of patients with genistein prior to the administration of SB715992 even better therapeutic strategy with less toxicity T by systemic SB715992. However, further detailed studies, including normal in vivo studies are required to causal Zusammenh length Between these genes and modifies treatment outcomes in animal models, and to establish in human patients. Malignant gliomas, the subtype h Most frequent primary Re brain tumors,