| Jinn-Shiun Chen, |
------>authors3_c=None ------>paper_class1=1 ------>Impact_Factor=3.000 ------>paper_class3=2 ------>paper_class2=1 ------>vol= ------>confirm_bywho=yangyuan ------>insert_bywho=hoyuansn ------>Jurnal_Rank=37.9 ------>authors4_c=None ------>comm_author=1 ------>patent_EDate=None ------>authors5_c=None ------>publish_day=None ------>paper_class2Letter=None ------>page2= ------>medlineContent= ------>unit=E0500 ------>insert_date=20051208 ------>iam=7 ------>update_date=None ------>author=??? ------>change_event=6 ------>ISSN=None ------>authors_c=None ------>score=500 ------>journal_name=Molecular Carcinogenesis ------>paper_name=Checkpoint kinase 1-mediated phosphorylation of Cdc25C and Bad proteins are involved in antitumor effects of loratadine-induced G2/M phase cell cycle arrest and apoptosis. ------>confirm_date=20061208 ------>tch_id=084007 ------>pmid=16649252 ------>page1= ------>fullAbstract=In this study, we first demonstrated that loratadine (LOR), a promising world widely used oral anti-histamine, effectively inhibits growth of tumors derived from human colon cancer cells (COLO 205) in an in vivo setting. In vitro study demonstrated that the anti-tumor effects of LOR in COLO 205 cells were mediated by causing G(2)/M phase cell growth cycle arrest and caspase 9-mediated apoptosis. Cell-cycle arrest induced by LOR (75 microM, 24 h) was associated with a significant decrease in protein levels of cyclin B1, cell division cycle (Cdc) 25B, and Cdc25C, leading to accumulation of Tyr-15-phosphorylated Cdc2 (inactive form). Interestingly, LOR (75 microM, for 4 h) treatment also resulted in a rapid and sustained phosphorylation of Cdc25C at Ser-216, leading to its translocation from the nucleus to the cytoplasm because of increased binding with 14-3-3. We further demonstrated that the LOR-induced Cdc25C (Ser-216) phosphorylation was blocked in the presence of checkpoint kinase 1 (Chk1) specific inhibitor (SB-218078). The cells treated with LOR in the presence of Chk1 specific inhibitor (SB-218078) were then released from G(2)/M arrest into apoptosis. These results implied that Chk1-mediated phosphorylation of Cdc25C plays a major role in response to LOR-mediated G(2)/M arrest. Although the Chk1-mediated cell growth arrest in response to DNA damage is well documented, our results presented in this study was the first report to describe the Chk1-mediated G(2)/M cell-cycle arrest by the histamine H1 antagonist, LOR. ------>tmu_sno=None ------>sno=12088 ------>authors2=Shyr-Yi Lin, ------>authors3=Wei-Ling Tso, ------>authors4=Geng-Chang Yeh, ------>authors5=Wen-Sen Lee, ------>authors6=How Tseng, Li-Ching Chen, and Yuan-Soon Ho ------>authors6_c=None ------>authors=Jinn-Shiun Chen, ------>delete_flag=0 ------>SCI_JNo=None ------>authors2_c=None ------>publish_area=None ------>updateTitle=Checkpoint kinase 1-mediated phosphorylation of Cdc25C and bad proteins are involved in antitumor effects of loratadine-induced G2/M phase cell-cycle arrest and apoptosis. ------>language=2 ------>check_flag=None ------>submit_date=None ------>country=None ------>no= ------>patent_SDate=None ------>update_bywho=None ------>publish_year=2005 ------>submit_flag=None ------>publish_month=None |