PMID- 16297711
OWN - NLM
STAT- MEDLINE
DCOM- 20060302
LR  - 20151119
IS  - 0304-3835 (Print)
IS  - 0304-3835 (Linking)
VI  - 230
IP  - 2
DP  - 2005 Dec 18
TI  - Involvement of Bcl-2 family, cytochrome c and caspase 3 in induction of apoptosis 
      by beauvericin in human non-small cell lung cancer cells.
PG  - 248-59
AB  - Beauvericin (BEA), a cyclic hexadepsipeptide from Codyceps cicadae, possesses 
      anti-convulsion, anti-arrhythmia, sedation, and anti-tumor activities. It has 
      been reported that BEA induces apoptosis in several cancer cell lines. However, 
      the molecular mechanism underlying the BEA-induced apoptotic process is not yet 
      clearly understood. In the present study, the intracellular signaling pathways of 
      BEA-induced apoptosis in human non-small cell lung cancer (NSCLC) A549 cells were 
      investigated using morphological analysis and terminal deoxynucleotidyl 
      transferase dUTP nick-end labeling (TUNEL) technique. In this study, BEA-induced 
      apoptosis in human NSCLC A549 cells demonstrated a BEA concentration- and 
      treatment time-dependent manner. This BEA-induced apoptosis in human NSCLC A549 
      cells was also accompanied by the up-regulation of Bax, Bak, and p-Bad and 
      down-regulation of p-Bcl-2, but no effect on the levels of Bcl-X(L) or Bad 
      proteins. Moreover, the BEA treatment resulted in a significant reduction of 
      mitochondrial membrane potential, increase in the release of mitochondrial 
      cytochrome c (cyt c), and activation of caspase 3. Furthermore, treatment with 
      caspase 3 inhibitor (z-DEVD-fmk) was capable to prevent the BEA-induced caspase 3 
      activity and cell death. These results clearly demonstrate that the induction of 
      apoptosis by BEA involves multiple cellular/molecular pathways and strongly 
      suggest that pro- and anti-apoptotic Bcl-2 family proteins, mitochondrial 
      membrane potential, mitochondrial cyt c, and caspase 3, they all participate in 
      BEA-induced apoptotic process in human NSCLC A549 cells.
FAU - Lin, Hen-I
AU  - Lin HI
AD  - School of Medicine, Fu Jen Catholic University, 510, Chung-Cheng Road, 
      Hsin-Chuang, Taipei Hsien 242, Taiwan.
FAU - Lee, Yih-Jing
AU  - Lee YJ
FAU - Chen, Bing-Fang
AU  - Chen BF
FAU - Tsai, Meng-Chao
AU  - Tsai MC
FAU - Lu, Jen-Lin
AU  - Lu JL
FAU - Chou, Cheng-Jen
AU  - Chou CJ
FAU - Jow, Guey-Mei
AU  - Jow GM
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Ireland
TA  - Cancer Lett
JT  - Cancer letters
JID - 7600053
RN  - 0 (Antineoplastic Agents)
RN  - 0 (Depsipeptides)
RN  - 0 (Proto-Oncogene Proteins c-bcl-2)
RN  - 26S048LS2R (beauvericin)
RN  - 9007-43-6 (Cytochromes c)
RN  - EC 3.4.22.- (CASP3 protein, human)
RN  - EC 3.4.22.- (Caspase 3)
RN  - EC 3.4.22.- (Caspases)
SB  - IM
MH  - Antineoplastic Agents/*pharmacology
MH  - *Apoptosis
MH  - Carcinoma, Non-Small-Cell Lung
MH  - Caspase 3
MH  - Caspases/metabolism
MH  - Cell Line, Tumor
MH  - Cell Survival/drug effects
MH  - Cytochromes c/metabolism
MH  - DNA Fragmentation
MH  - Depsipeptides/*pharmacology
MH  - Humans
MH  - In Situ Nick-End Labeling
MH  - Lung Neoplasms
MH  - Membrane Potentials/drug effects
MH  - Mitochondria/drug effects/metabolism/physiology
MH  - Proto-Oncogene Proteins c-bcl-2/metabolism
EDAT- 2005/11/22 09:00
MHDA- 2006/03/03 09:00
CRDT- 2005/11/22 09:00
PHST- 2004/11/30 00:00 [received]
PHST- 2004/12/27 00:00 [revised]
PHST- 2004/12/29 00:00 [accepted]
PHST- 2005/11/22 09:00 [pubmed]
PHST- 2006/03/03 09:00 [medline]
PHST- 2005/11/22 09:00 [entrez]
AID - S0304-3835(05)00012-1 [pii]
AID - 10.1016/j.canlet.2004.12.044 [doi]
PST - ppublish
SO  - Cancer Lett. 2005 Dec 18;230(2):248-59. doi: 10.1016/j.canlet.2004.12.044.