Document Detail


Endostar induces apoptotic effects in HUVECs through activation of caspase-3 and decrease of Bcl-2.
MedLine Citation:
PMID:  19331180     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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.
Authors:
Yun Ling; Na Lu; Ying Gao; Yan Chen; Sen Wang; Yong Yang; Qinglong Guo
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Anticancer research     Volume:  29     ISSN:  0250-7005     ISO Abbreviation:  Anticancer Res.     Publication Date:  2009 Jan 
Date Detail:
Created Date:  2009-03-31     Completed Date:  2009-04-16     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  8102988     Medline TA:  Anticancer Res     Country:  Greece    
Other Details:
Languages:  eng     Pagination:  411-7     Citation Subset:  IM    
Affiliation:
Jiangsu Key Laboratory of Carcinogenesis and Intervention, China Pharmaceutical University, Nanjing 210009 People's Republic of China.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:
Caspase 3 / metabolism*
Cells, Cultured
Endostatins / pharmacology*
Endothelial Cells / cytology,  drug effects*,  metabolism
Enzyme Activation / drug effects
Humans
Proto-Oncogene Proteins c-bcl-2 / biosynthesis*
Recombinant Proteins / pharmacology
bcl-2-Associated X Protein / biosynthesis
Chemical
Reg. No./Substance:
0/BAX protein, human; 0/Endostatins; 0/Proto-Oncogene Proteins c-bcl-2; 0/Recombinant Proteins; 0/bcl-2-Associated X Protein; 0/endostar protein; EC 3.4.22.-/Caspase 3

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


Previous Document:  Synthetic inhibitors of galectin-1 and -3 selectively modulate homotypic cell aggregation and tumor ...
Next Document:  Release of volatile organic compounds from the lung cancer cell line NCI-H2087 in vitro.