| Huang HM* |
------>authors3_c= ------>paper_class1=1 ------>Impact_Factor=3.643 ------>paper_class3=2 ------>paper_class2=1 ------>vol=218 ------>confirm_bywho=wslee ------>insert_bywho=cmbhhm ------>Jurnal_Rank=28.2 ------>authors4_c= ------>comm_author=1 ------>patent_EDate=None ------>authors5_c= ------>publish_day=1 ------>paper_class2Letter=None ------>page2=574 ------>medlineContent= ------>unit=E1300 ------>insert_date=20081121 ------>iam=1 ------>update_date=None ------>author=??? ------>change_event=4 ------>ISSN= ------>authors_c= ------>score=500 ------>journal_name=Journal of Cellular Physiology ------>paper_name=c-Jun blocks cell differentiation but not growth inhibition or apoptosis of chronic myelogenous leukemia cells induced by STI571 and by histone deacetylase inhibitors ------>confirm_date=20090507 ------>tch_id=089027 ------>pmid=19006173 ------>page1=568 ------>fullAbstract=The constitutively active Bcr-Abl tyrosine kinase plays a crucial role in chronic myelogenous leukemia (CML) pathogenesis. The Bcr-Abl protein induces the upregulation of proto-oncogene c-Jun, which is involved in Bcr-Abl transforming activity in Bcr-Abl positive cells. Recent studies reported that c-Jun inhibited hemoglobin synthesis in human CML cell line K562. However, c-Jun also plays a critical role in cell proliferation and apoptosis. In this study, we investigated the physiological roles of c-Jun in cell proliferation, apoptosis and erythroid differentiation of K562 cells. Firstly, we generated K562 cell lines stably overexpressing c-Jun. These clones have the same proliferation rate as the parental cell line in general culture medium. Endogenous c-Jun expression was analyzed to determine the effective concentration of STI571 for inhibiting Bcr-Abl signaling. Western blots show that STI571 inhibited c-Jun expression in a dose-dependent manner, reaching a maximum inhibition at 1 microM. STI571 could inhibit c-Jun expression in K562 cells, but not in c-Jun-overexpression cells. c-Jun did not alter growth inhibition and apoptotic induction by STI571 treatment, but inhibited STI571-induced erythroid differentiation. Moreover, c-Jun did not alter growth inhibition and apoptotic induction by histone deacetylase (HDAC) inhibitors (apicidin, sodium butyrate, and MS275) treatment, but inhibited HDAC inhibitors-induced erythroid differentiation. These results suggest that c-Jun may modulate anticancer drugs-induced cell differentiation but not growth inhibition and apoptosis in CML cells. ------>tmu_sno=None ------>sno=19734 ------>authors2=Liu JC ------>authors3= ------>authors4= ------>authors5= ------>authors6= ------>authors6_c= ------>authors=Huang HM* ------>delete_flag=0 ------>SCI_JNo=None ------>authors2_c= ------>publish_area=0 ------>updateTitle=c-Jun blocks cell differentiation but not growth inhibition or apoptosis of chronic myelogenous leukemia cells induced by STI571 and by histone deacetylase inhibitors. ------>language=2 ------>check_flag=None ------>submit_date=None ------>country=None ------>no=00 ------>patent_SDate=None ------>update_bywho=None ------>publish_year=2009 ------>submit_flag=None ------>publish_month=3 |