In both hormones depleted condition to be treated and DHT, suggesting the involvement of cell proliferation castration-AR, as in the previous Ver Described ffentlichung. Interestingly, treatment inhibits cell proliferation CEP-18770 more effectively than siTACC2 LTAD ISEA. TACC2 growthinhibition was even clearer in a hormone-depleted state. In addition, k More than nnte ISEA siTACC2 treated cells did not significantly inhibit cell proliferation castration. To the R For analysis by each TACC2 in the cell cycle progression, we have cells synchronized in G0/G1 phase and G2 / M. We FACS analysis led after leaving the cell cycle. We observed significant transfected G2 / M accumulation and a decrease in the percentage of cells in S phase in cells with LTAD siTACC2, 24 h after release from synchronization G0/G1 phase. This suggests that the inhibition of cell cycle occurs in the G2 / M, we also showed that the robust MEK Signaling Pathway decrease caused the percentage of cells in S phase by TACC2 surcharge after G2 / M synchronization nnten k. Moreover, we have also shown that TACC2 surcharge cell proliferation of DU145 cells, AR-independent Ngigen inhibits prostate cancer cell line. Thus TACC2 is required hormonrefrakt cell proliferation of both hormone-sensitive positive and negative AR AR Ren cell lines from prostate cancer. Treated for further analysis of the properties of mitotic cells with LTAD siTACC2, we have Immunofluorescence analysis of these cells using anti-tubulin and anti TACC2, centrosome marker. TACC2 knockdown reduced tubulin-F Staining of centrosomes in most cells or mitotic cells showed abnormal mitotic spindles with more than two centrosomes, or simply, f Controlled while in the cells Disable the two centrosomes were detected in cells in mitosis. It is also in cells incubated with LTAD siTACC2 Board, we observed an instability t chromatin w During mitosis. An overexpression of
TACC2 f Promotes cell cycle at the G2 / M phase additives Tzlich we examined whether overexpression TACC2 plays The oncogene in prostate cancer. We generated expressing LNCaP cells F Is stable and best CONFIRMS TACC2 TACC2 exogenous expression by Western blot analysis. These cells overexpress TACC2 increased faster than the parental LNCaP cells. We also observed the reactivity Ability of androgen-cell proliferation in LNCaP cells overexpressing TACC2 of an Etoposide STD test. This result implies that the AR functions to improve almost normal cell proliferation in LNCaP cells overexpressing TACC2. To investigate the effect of raising the level of expression TACC2 to investigate the cell cycle, we synchronized cells and was cell-cycle analysis was performed. Was no significant difference in cyclin D1 induction, which is important for the G1 / S transition after release from G0/G1 arrest by Rinderf Tenserum treatment, and observed between vectors expressing cells overexpress TACC2. Zus Tzlich showed FACS analysis, no significant Ver Change after synchronization at G0/G1. However, after G2 / M synchronization, we observed a rapid induction of cyclin D1 overexpressing cells, cells as compared to TACC2 vectorexpressing. In addition, by FACS analysis 24 hours after the release from G2 / M arrest, we identified a significant decrease in G2/Mphase cells and accumulation of cells in S phase. These data suggest that TACC2 ceiling.