TY - JOUR T1 - Endostar Induces Apoptotic Effects in HUVECs through Activation of Caspase-3 and Decrease of Bcl-2 JF - Anticancer Research JO - Anticancer Res SP - 411 LP - 417 VL - 29 IS - 1 AU - YUN LING AU - NA LU AU - YING GAO AU - YAN CHEN AU - SEN WANG AU - YONG YANG AU - QINGLONG GUO Y1 - 2009/01/01 UR - http://ar.iiarjournals.org/content/29/1/411.abstract N2 - Background: Endostar is a novel recombinant human endostatin expressed and purified in Escherichia coli with the N-terminal modified. It has been shown that endostar inhibited the proliferation of human umbilical vein endothelial cells (HUVECs) through the membrane surface receptor KDR/flt-1(VEGFR-2, vascular endothelial growth factor receptor-2) by exerting anti-angiogenesis effects. But the molecular mechanism remained unclear. Materials and Methods: The apoptotic effects induced by endostar in the serum-deprived situation were investigated by 4'-6-diaminidino-2-phenylindole (DAPI) staining and the Annexin V-fluorescein isothiocyanate (FITC) binding assay. The mechanism of action was explored by Western blotting assay. Results: Endostar induced remarkable apoptosis in HUVECs. The expressions of apoptosis-related proteins showed that caspase-3 was activated, but caspase-8, a marker of the non-mitochondria-mediated apoptosis signal pathway, was not. Further investigation revealed that cellular Bcl-2 decreased in the endostar-treated groups, while the level of Bax was almost unchanged. Conclusion: Endostar induces apoptotic effects in HUVECs through the activation of caspase-3 and a decrease of the Bcl-2 to Bax ratio. Copyright© 2009 International Institute of Anticancer Research (Dr. John G. Delinassios), All rights reserved ER -