Document Detail


Key regulators in bee venom-induced apoptosis are Bcl-2 and caspase-3 in human leukemic U937 cells through downregulation of ERK and Akt.
MedLine Citation:
PMID:  17052670     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Bee venom (BV) has been known to inhibit proliferation and induce apoptosis in cancer cells. However, the molecular mechanisms involved in BV-induced apoptosis are still uncharacterized in human leukemic cells. In the present study, we report that BV induces apoptosis in leukemic U937 cells through downregulation of ERK and Akt signal pathway. Furthermore, BV-induced apoptosis was accompanied by downregulation of Bcl-2, activation of caspase-3 and a subsequent poly(ADP-ribose)polymerase (PARP) cleavages. The induction of apoptosis also was accompanied by the downregulation of the inhibitor of apoptosis protein (IAP) family proteins. Caspase-3 inhibitor, z-DEVD-fmk, was significantly capable of restoring cell viability and BV-induced apoptosis through caspase-3 activation was significantly attenuated in Bcl-2-overexpressing cells. These results indicate that downregulation of Bcl-2 plays a major role in the initiation as an activator of a caspase-3 involved with BV-induced apoptosis. BV also triggered the activation of p38 MAPK and JNK, and downregulation of ERK and Akt. PD98059 (an inhibitor of ERK) or LY294002 (an inhibitor of Akt), but not an inhibitor of p38 MAPK and JNK, significantly decreased cell viability and increased lactate dehydrogenase (LDH) release. The results indicated that key regulators in BV-induced apoptosis are Bcl-2 and caspase-3 in human leukemic U937 cells through downregulation of the ERK and Akt signal pathway.
Authors:
Dong-Oh Moon; Sung-Yong Park; Moon-Soo Heo; Ki-Cheon Kim; Cheol Park; Woo Shin Ko; Yung Hyun Choi; Gi-Young Kim
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2006-08-22
Journal Detail:
Title:  International immunopharmacology     Volume:  6     ISSN:  1567-5769     ISO Abbreviation:  Int. Immunopharmacol.     Publication Date:  2006 Dec 
Date Detail:
Created Date:  2006-10-20     Completed Date:  2007-01-10     Revised Date:  2009-11-19    
Medline Journal Info:
Nlm Unique ID:  100965259     Medline TA:  Int Immunopharmacol     Country:  Netherlands    
Other Details:
Languages:  eng     Pagination:  1796-807     Citation Subset:  IM    
Affiliation:
Faculty of Applied Marine Science, Cheju National University, Jeju, South Korea.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:
Animals
Apoptosis / drug effects*
Bee Venoms / pharmacology*
Bone Marrow Cells
Caspase 3 / metabolism
Cell Proliferation / drug effects*
Cell Survival / drug effects
Collagen Type XI / metabolism
DNA Fragmentation
Down-Regulation
Extracellular Signal-Regulated MAP Kinases / metabolism
HL-60 Cells
Humans
K562 Cells
L-Lactate Dehydrogenase / metabolism
Mice
Mice, Inbred C57BL
Proto-Oncogene Proteins c-akt / metabolism
Proto-Oncogene Proteins c-bcl-2 / metabolism
U937 Cells
Chemical
Reg. No./Substance:
0/Bee Venoms; 0/COL11A2 protein, human; 0/Collagen Type XI; 0/Proto-Oncogene Proteins c-bcl-2; EC 1.1.1.27/L-Lactate Dehydrogenase; EC 2.7.11.1/Proto-Oncogene Proteins c-akt; EC 2.7.11.24/Extracellular Signal-Regulated MAP Kinases; EC 3.4.22.-/Caspase 3

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


Previous Document:  Inhibition of ICAM-1 expression by garlic component, allicin, in gamma-irradiated human vascular end...
Next Document:  Toll-like receptor 2-dependent activation of monocytes by Spirulina polysaccharide and its immune en...