Hsu YF |
------>authors3_c=??? ------>paper_class1=1 ------>Impact_Factor=2.371 ------>paper_class3=2 ------>paper_class2=1 ------>vol=46 ------>confirm_bywho=chlin ------>insert_bywho=wslee ------>Jurnal_Rank=49.0 ------>authors4_c=??? ------>comm_author=1 ------>patent_EDate=None ------>authors5_c=??? ------>publish_day=1 ------>paper_class2Letter=None ------>page2=283 ------>medlineContent= ------>unit=E1300 ------>insert_date=20071217 ------>iam=1 ------>update_date=None ------>author=??? ------>change_event=4 ------>ISSN= ------>authors_c=??? ------>score=500 ------>journal_name=Mol. Carcinog ------>paper_name=Involvement of Ras/Raf-1/Erk actions in the magnolol-induced upregulation of p21 and cell cycle arrest in colon cancer cells. ------>confirm_date=20071217 ------>tch_id=086001 ------>pmid=17295239 ------>page1=275 ------>fullAbstract=Previously, we showed that magnolol induces cell-cycle arrest in cultured colon and liver cancer cells through an upregulation of the p21 protein. The aim of this study was to delineate the molecular mechanism underlying this magnolol-induced increase of p21 protein. Thus our RT-PCR analysis demonstrated that the mRNA levels of p21 were increased at 1 h after magnolol treatment and sustained for at least 24 h. The p21 promoter activity was also increased by magnolol treatment. Western blot analysis demonstrated that treatment of COLO-205 cells with magnolol increased the levels of phosphorylation of extracellular signal-regulated kinase (ERK). Pretreatment of the cells with PD98059 abolished the magnolol-induced upregulation of p21 protein, suggesting the involvement of an ERK pathway in the magnolol-induced upregulation of p21 in COLO-205 cells. Ras inhibitor peptide abolished the magnolol-induced increase of phosphorylated ERK protein levels, increase of p21 protein, and decrease of thymidine incorporation. Moreover, treatment of COLO-205 with magnolol increased the phosphorylated Raf-1 protein (the Ras target molecule). Pretreatment of the cells with Raf-1 inhibitor reversed the magnolol-induced decrease in thymidine incorporation. Treatment of the cells with CaM kinase inhibitor, but not protein kinase A (PKA) inhibitor or phosphatidylinosital 3-kinase (PI3K) inhibitor, abolished the magnolol-induced activation of ERK and decrease of thymidine incorporation. Taken together, our results suggest that magnolol activates ERK phosphorylation through a Ras/Raf-1-mediated pathway. Subsequently, p21 expression is increased, and finally thymidine incorporation is decreased. ------>tmu_sno=None ------>sno=16480 ------>authors2=Lee TS ------>authors3=Lin SY ------>authors4=Hsu SP ------>authors5=Juan SH ------>authors6=Hsu YH, Zhong WB, Lee WS ------>authors6_c=???, ???, ??? ------>authors=Hsu YF ------>delete_flag=0 ------>SCI_JNo=None ------>authors2_c=??? ------>publish_area=0 ------>updateTitle=Involvement of Ras/Raf-1/ERK actions in the magnolol-induced upregulation of p21 and cell-cycle arrest in colon cancer cells. ------>language=2 ------>check_flag=None ------>submit_date=None ------>country=None ------>no= ------>patent_SDate=None ------>update_bywho=None ------>publish_year=2007 ------>submit_flag=None ------>publish_month=1 |