Steven Kuan-Hua Hu |
------>authors3_c= ------>paper_class1=1 ------>Impact_Factor=2.691 ------>paper_class3=2 ------>paper_class2=1 ------>vol= ------>confirm_bywho=curator ------>insert_bywho=tonyliu ------>Jurnal_Rank=16.0 ------>authors4_c= ------>comm_author= ------>patent_EDate=None ------>authors5_c= ------>publish_day=1 ------>paper_class2Letter=None ------>page2= ------>medlineContent= ------>unit=F0400 ------>insert_date=20060419 ------>iam=3 ------>update_date=None ------>author=??? ------>change_event=4 ------>ISSN= ------>authors_c= ------>score=500 ------>journal_name=Toxicology ------>paper_name=Cantharidin-Induced Cytotoxicity and Cyclooxygenase 2 Expression in Human Bladder Carcinoma Cell Line ------>confirm_date=20061221 ------>tch_id=090026 ------>pmid=16697099 ------>page1= ------>fullAbstract=Mylabris is used in clinical therapy, but is always accompanied by cystitis. The toxic effects of mylabris on bladder are attributed to its active principle: cantharidin. In the present study, we explored how cantharidin induces cytotoxicity in the bladder. Human bladder carcinoma cell line T 24 cells were used as target cells, and human colon carcinoma HT 29 cells as native cells. Cantharidin exhibited acute cytotoxicity in the T 24 cells, and IC(50) was 21.8, 11.2 and 4.6 microM after treatment for 6, 24 and 48 h, respectively. The cytotoxicity of cantharidin was not significantly enhanced when T 24 cells were treated for a longer time. Moreover, PARP proteins and pro-caspase 3, Bcl-2 were significantly inhibited after cantharidin treatment in T 24 cells. Pretreatment with the caspase 3 inhibitor markedly inhibited cantharidin-induced cell death. Therefore, we suggested that cantharidin could induce apoptosis via active caspase 3 in T 24 cells. When T 24 cells were treated with cantharidin at a low dose, the cell cycle was arrested in the G(2)/M phase. Furthermore, p21(Cip1/Waf1) was enhanced, and cyclin A, B1 and cdk1 decreased. At a high dose (more 12.5 microM), cantharidin could stimulate T 24 cells to deplete a large number of ATP and induce secondary necrosis. In addition, cantharidin also stimulated COX 2 over-expression and PGE(2) production in T 24 cells, in a dose-dependent manner. However, cantharidin also induced apoptosis and G(2)/M phase arrest in HT 29 cells, but did not induce COX 2 over-expression. Therefore, we suggest that cantharidin may induce cystitis through secondary necrosis and COX 2 over-expression. ------>tmu_sno=None ------>sno=13383 ------>authors2=Hao-Hsien Lee ------>authors3=Der-Zen Liu ------>authors4=Chien-Chih Wu ------>authors5=Ching-Chiung Wang ------>authors6= ------>authors6_c= ------>authors=Steven Kuan-Hua Hu ------>delete_flag=0 ------>SCI_JNo=None ------>authors2_c= ------>publish_area=0 ------>updateTitle=Cantharidin-induced cytotoxicity and cyclooxygenase 2 expression in human bladder carcinoma cell line. ------>language=2 ------>check_flag=None ------>submit_date=None ------>country=None ------>no= ------>patent_SDate=None ------>update_bywho=None ------>publish_year=2006 ------>submit_flag=None ------>publish_month=1 |