Rock Creek Pharmaceuticals Inc. (fka RCPIQ)

[Buddhahead]

Celastrol induces apoptosis of gastric cancer cells by miR-146a inhibition of NF-?B activity in Cancer Cell International 2013,, Min Sha, Jun Ye, Li-xin Zhang, Zheng-yun Luan and Ya-bao Chen*, Institute of Clinical medicine, Taizhou people’s Hospital affiliated of Nantong University of medicine, 210 Yingchun, Taizhou, Jiangsu Province, 225300, China

Celastrol is a remedial ingredient isolated from the root extracts of Tripterygium Wilfordi (Thunder of God vine) and Celastrus Regelii. In in vitro and in vivo animal experiments, celastrol exhibits antioxidant,[2] anti-inflammatory,[3][4] anticancer,[5][6][7][8] and insecticidal [9] activities. Celastrol, also known as tripterine, is a pentacyclic triterpenoid and belongs in the family of quinone methides.(Wikipedia)

IMPORTANT REFERENCE NOT CITED IN ARTICLE: Michael Mullan, Roskamp Institute:
Reduction of ß-amyloid pathology by celastrol in a transgenic mouse model of Alzheimer's disease
Daniel Paris,corresponding author1 Nowell J Ganey,1 Vincent Laporte,1 Nikunj S Patel,1 David Beaulieu-Abdelahad,1 Corbin Bachmeier,1 Amelia March,1 Ghania Ait-Ghezala,1 and Michael J Mullan1
1The Roskamp Institute, 2040 Whitfield Avenue, Sarasota, FL 34243, USA
corresponding authorCorresponding author.
Daniel Paris: [e-mail]; Nowell J Ganey: [e-mail]; Vincent Laporte: [e-mail]; Nikunj S Patel: [e-mail]; David Beaulieu-Abdelahad: [e-mail]; Corbin Bachmeier: [e-mail]; Amelia March: [e-mail]; Ghania Ait-Ghezala: [e-mail]; Michael J Mullan: [e-mail]
Received December 17, 2009; Accepted March 8, 2010.

Article at:
http://pubmedcentralcanada.ca/pmcc/articles/PMC2841120/


Abstract:
Background
Celastrol, a plant triterpene, is known to play important role in inhibiting proliferation and inducing apoptosis of gastric cancer cells. In the present study, the mechanism of celastrol on gastric cancer cells apoptosis was examined.

Methods
We assessed effect of celastrol on NF-?B signaling pathway in gastric cancer cells using western blot and luciferase reporter assay. The real-time PCR was used to evaluate the effect of celastrol on miR-146a expression, and miR-146a mimic to evaluate whether over-expression of miR-146a can affect NF-?B activity. Finally, the effect of miR-146a on celastrol-induced anti-tumor activity was assessed using miR-146a inhibitor.

Results
Celastrol decreased gastric cancer cells viability in a dose-dependent. Celastrol also reduced I?B phosphorylation, nuclear P65 protein levels and NF-?B activity. Furthermore, Celastrol could increase miR-146a expression and up-regulation of miR-146a expression could suppress NF-?B activity. More important, down-regulation of miR-146a expression can reverse the effect of celastrol on NF-?B activity and apoptosis in gastric cancer cells.

Conclusions
In this study, we demonstrated that the effect of celastrol on apoptosis is due to miR-146a inhibition of NF-?B activity.

Article at:
http://www.cancerci.com/content/13/1/50