Gene downstream Rts of the progression of prostate cancer modulated. The family of proteins TACC contain C-terminal coiled-coil TH-302 dome Tions and the development of cancer through its role in the formation of the mitotic spindle w Involved during mitosis. With regard to the functions of the TACC, TACC1 and TACC3 has been shown to exert r oncogenes in tumors TACC1 f Promotes transformation and mammary tumorigenesis in a mouse model, and TACC3 is regulated in various cancer cells. TACC3 aberrations have also been reported in patients with ovarian cancer and non-small cell lung cancer. TACC2 was originally developed as a potential tumor suppressor gene in breast cancer cells identified, although its R In the biological formation of tumors is controversial, because a recently published Ffentlichter report showed that TACC2 correlated with poor prognosis in patients with breast cancer. Our results showed that plays a TACC2 Oncogene of clinical prostate cancer tissues. The molecule is an independent Ngiger prognostic factor in prostate cancer Bev Lkerung that we examined in this study. The resistance to hormone therapy is still a big clinical problem in prostate cancer there. Increasing evidence suggests that AR plays a role Significant at the transition to castration resistance to proliferation. For example, the AR amplification, hypersensitivity toward lower androgen levels in prostate tissue, bidirectional p38 MAPK Signaling Pathway cross-talk between the signaling pathway of growth factor receptor, AR, and AR variants are the most important mechanisms that were suggested above. In this study, we have a model of castration-resistant prostate cancer with androgen deprivation in the long run. Best in cells LTAD We saturated that AR expression was significantly regulated. Although the dependent Independent
DHT for the regulation of TMPRSS2 mRNA in cells is not significant compared to parental LNCaP cells LTAD, occupied by DHT regulates mRNA expression of target genes of other androgens, even at low concentrations, such as the APA and ARFGAP3 We previously considered androgen responsive wachstumsf rdernde identified factors. These data suggest that the increased Androgensensitivit t, at least in the transcriptional regulation of gene promoters in the cells of several LTAD compared to parental LNCaP cells Ht. Therefore, we expect that our cell model system to study an appropriate LTAD the molecular mechanisms of development of CRPC is. We have shown TACC2 expression of both the absence and presence of DHT and hypersensitivity TACC2 induction in cells of the LTAD. Because the crew AR to Bergenin ARBS TACC2 was found that increased in the basal cells of the two countries and LTAD stimulating hormone Ht be, AR TACC2 in control cells was LTAD LTAD AR cells demonstrated Ersch Pft. In addition treatment inhibits cell proliferation siTACC2 clearly than Siar, and the addition of ISEA siTACC2 untreated cells, the in It has changed, is significant cell proliferation. These data suggest that m for may have a play TACC2 r The amplified signal AR important role in castration resistance. The data VER Published ChIP Seq support this proposal because the enrichment of AR binding to TACC2 ARBS also shown in metastatic prostate cancer tissues, as well as lines of androgen-sensitive prostate cancer cells. Acceleration of tumor formation by overexpression in TACC2 castrated nude.