| Wu MP |
------>authors3_c=??? ------>paper_class1=1 ------>Impact_Factor=5.366 ------>paper_class3=2 ------>paper_class2=1 ------>vol=29 ------>confirm_bywho=tzengcr ------>insert_bywho=mpwu ------>Jurnal_Rank=14.2 ------>authors4_c=??? ------>comm_author= ------>patent_EDate=None ------>authors5_c=??? ------>publish_day=1 ------>paper_class2Letter=None ------>page2=1123 ------>medlineContent= ------>unit=E0111 ------>insert_date=20080321 ------>iam=1 ------>update_date=None ------>author=??? ------>change_event=4 ------>ISSN= ------>authors_c=??? ------>score=465 ------>journal_name=Carcinogenesis ------>paper_name=A novel role of thrombospondin-1 in cervical cervical carcinogenesis: Inhibit stroma reaction by inhibiting activated firbroblats from invading cancer ------>confirm_date=20081205 ------>tch_id=093043 ------>pmid=18413367 ------>page1=1115 ------>fullAbstract=Thrombospondin (TSP)-1, a potent angiogenesis inhibitor, has been shown to exert different biological functions on various cell types. Here, we investigate the role of TSP-1 in tumor-stroma reaction, which is mainly characterized by fibroblast activation to create a permissive microenvironment for tumor progression. Immunohistochemistry examinations in the human surgical specimens have shown that a downregulation of TSP-1 during the progression of cervical carcinogenesis was accompanied by an emergence in the upregulation of stroma markers, alpha-smooth muscle actin (alpha-SMA) and desmin. Transfection of SiHa cervical cancer cells with a plasmid expressing the TSP-1 protein exhibited antiangiogenic activity in vitro and resulted in reduced tumor growth in severe combined immunodeficiency (SCID) mice, which was accompanied by a decrease in tumor vascularization and lower expressions of alpha-SMA and desmin than those in the vector controls. Transfection with TSP-1 and purified TSP-1 added to NIH3T3 cells did not alter the protein levels of alpha-SMA and desmin but significantly inhibited matrix metalloprotease-2 activity. Transforming growth factor-beta (TGF-beta), a major factor in the activation of fibroblasts, increased alpha-SMA and desmin expression and the ability of cell migration and invasion in NIH3T3 cells. The increased migration ability and the invasive ability into tumor cluster of TGF-beta-treated NIH3T3 cells were dose dependently inhibited by TSP-1. In contrast, ectopic TSP-1 expression in SiHa cells has little effect on the invasive ability of the NIH3T3 cells. Together, our findings demonstrate a novel role of TSP-1 to inhibit tumor-stroma reaction that could be attributed to the blockage of activated fibroblasts from invading cancer cells. ------>tmu_sno=None ------>sno=17132 ------>authors2=Young MJ ------>authors3=Tzeng CC ------>authors4=Tzeng CR ------>authors5=Huang KF ------>authors6=Wu LW, Chou CY ------>authors6_c=???,??? ------>authors=Wu MP ------>delete_flag=0 ------>SCI_JNo=None ------>authors2_c=??? ------>publish_area=0 ------>updateTitle=A novel role of thrombospondin-1 in cervical carcinogenesis: inhibit stroma reaction by inhibiting activated fibroblasts from invading cancer. ------>language=2 ------>check_flag=None ------>submit_date=None ------>country=None ------>no= ------>patent_SDate=None ------>update_bywho=None ------>publish_year=2008 ------>submit_flag=None ------>publish_month=11 |