PMID- 21682651
OWN - NLM
STAT- MEDLINE
DCOM- 20120416
LR  - 20220317
IS  - 1532-2513 (Electronic)
IS  - 0892-3973 (Linking)
VI  - 34
IP  - 1
DP  - 2012 Feb
TI  - Andrographolide induces apoptosis in B16F-10 melanoma cells by inhibiting 
      NF-kappaB-mediated bcl-2 activation and modulating p53-induced caspase-3 gene 
      expression.
PG  - 143-51
LID - 10.3109/08923973.2011.588233 [doi]
AB  - Cancer is a disorder characterized by uncontrolled proliferation and reduced 
      apoptosis. Inducing apoptosis is an efficient method of treating cancers. In this 
      study, we investigated the effect of andrographolide on the induction of 
      apoptosis as well as its regulatory effect on the activation of transcription 
      factors in B16F-10 melanoma cells. Treatment of B16F-10 cells with nontoxic 
      concentration of andrographolide showed the presence of apoptotic bodies and 
      induced DNA fragmentation in a dose-dependent manner. Cell cycle analysis and 
      terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) assays also 
      confirmed the observation. The proapoptotic genes p53, Bax, caspase-9, and 
      caspase-3 were found upregulated in andrographolide-treated cells, whereas the 
      antiapoptotic gene bcl-2 was downregulated. This study also reveals that 
      andrographolide treatment could alter the production and expression of 
      proinflammatory cytokines and could inhibit the activation and nuclear 
      translocation of p65, p50, and c-Rel subunits of nuclear factor-kappaB (NF-kappaB), and 
      other transcription factors such as c-fos, activated transcription factor-2, and 
      cyclic adenosine monophosphate response element-binding protein in B16F-10 
      melanoma cells. These results suggest that andrographolide induces apoptosis via 
      inhibiting NF-kappaB-induced bcl-2-mediated survival signaling and modulating 
      p53-induced caspase-3-mediated proapoptotic signaling.
FAU - Pratheeshkumar, P
AU  - Pratheeshkumar P
AD  - Amala Cancer Research Centre, Amala Nagar, Thrissur, Kerala, India.
FAU - Sheeja, K
AU  - Sheeja K
FAU - Kuttan, Girija
AU  - Kuttan G
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20110620
PL  - England
TA  - Immunopharmacol Immunotoxicol
JT  - Immunopharmacology and immunotoxicology
JID - 8800150
RN  - 0 (ATF2 protein, human)
RN  - 0 (Activating Transcription Factor 2)
RN  - 0 (Anti-Inflammatory Agents)
RN  - 0 (BAX protein, human)
RN  - 0 (Diterpenes)
RN  - 0 (NF-kappa B)
RN  - 0 (Proto-Oncogene Proteins c-bcl-2)
RN  - 0 (Proto-Oncogene Proteins c-fos)
RN  - 0 (TP53 protein, human)
RN  - 0 (Tumor Suppressor Protein p53)
RN  - 0 (bcl-2-Associated X Protein)
RN  - 410105JHGR (andrographolide)
RN  - EC 3.4.22.- (CASP3 protein, human)
RN  - EC 3.4.22.- (CASP9 protein, human)
RN  - EC 3.4.22.- (Caspase 3)
RN  - EC 3.4.22.- (Caspase 9)
SB  - IM
MH  - Activating Transcription Factor 2/metabolism
MH  - Anti-Inflammatory Agents/*pharmacology
MH  - Apoptosis/*drug effects
MH  - Caspase 3/*biosynthesis
MH  - Caspase 9/metabolism
MH  - Cell Line, Tumor
MH  - Diterpenes/*pharmacology
MH  - Gene Expression Regulation, Enzymologic/*drug effects
MH  - Gene Expression Regulation, Neoplastic/*drug effects
MH  - Humans
MH  - Melanoma/*metabolism
MH  - NF-kappa B/*metabolism
MH  - Proto-Oncogene Proteins c-bcl-2/*metabolism
MH  - Proto-Oncogene Proteins c-fos/metabolism
MH  - Tumor Suppressor Protein p53/*metabolism
MH  - bcl-2-Associated X Protein/metabolism
EDAT- 2011/06/21 06:00
MHDA- 2012/04/17 06:00
CRDT- 2011/06/21 06:00
PHST- 2011/06/21 06:00 [entrez]
PHST- 2011/06/21 06:00 [pubmed]
PHST- 2012/04/17 06:00 [medline]
AID - 10.3109/08923973.2011.588233 [doi]
PST - ppublish
SO  - Immunopharmacol Immunotoxicol. 2012 Feb;34(1):143-51. doi: 
      10.3109/08923973.2011.588233. Epub 2011 Jun 20.