title: Endostar induces apoptotic effects in HUVECs through activation of caspase-3 and decrease of Bcl-2.
abstract: 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.
  
  
  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.
  
  
  CONCLUSIONS
  Endostar induces apoptotic effects in HUVECs through the activation of caspase-3 and a decrease of the Bcl-2 to Bax ratio.
authors.affiliation: Jiangsu Key Laboratory of Carcinogenesis and Intervention, China Pharmaceutical University, Nanjing 210009 People's Republic of China.
authors.forename: Yun
authors.initials: Y
authors.lastname: Ling
authors.forename: Na
authors.initials: N
authors.lastname: Lu
authors.forename: Ying
authors.initials: Y
authors.lastname: Gao
authors.forename: Yan
authors.initials: Y
authors.lastname: Chen
authors.forename: Sen
authors.initials: S
authors.lastname: Wang
authors.forename: Yong
authors.initials: Y
authors.lastname: Yang
authors.forename: Qinglong
authors.initials: Q
authors.lastname: Guo