Abstract | BACKGROUND: METHODS: Efficacy of four different doses in parts per million of celecoxib, such as 200 ppm, 400 ppm, 600 ppm, and 1,000 ppm representing very low, moderate, and high doses, respectively were tested against adenocarcinoma of the mouse prostate using a transgenic adenocarcinoma of the mouse prostate (TRAMP) model assay. RESULTS: Dietary supplement of celecoxib at doses of 400 ppm, 600 ppm, and 1,000 ppm are most effective against mPIN (mouse prostatic intraepithelial neoplasia) and adenocarcinoma of the prostate. Tumor growth inhibition by celecoxib was associated with increased rate of apoptosis. At 1,000 ppm, a complete inhibition of the PIN lesions was extended to limit the growth of adenocarcinoma (from 85% to 15%) and metastasis of the mouse prostate. The chemopreventive effect was significant (P<0.01) at 400 ppm, 600 ppm, and 1,000 ppm doses compared to that at the lowest dose of 200 ppm and control. A dose-dependent effect on tumor growth inhibition was associated with reduced expression of NF-kappaBp65 and COX-2. CONCLUSIONS:
|
Authors | Bhagavathi A Narayanan, Narayanan K Narayanan, Brian Pttman, Bandaru S Reddy |
Journal | The Prostate
(Prostate)
Vol. 66
Issue 3
Pg. 257-65
(Feb 15 2006)
ISSN: 0270-4137 [Print] United States |
PMID | 16175586
(Publication Type: Journal Article, Research Support, N.I.H., Extramural, Research Support, Non-U.S. Gov't)
|
Copyright | Copyright (c) 2005 Wiley-Liss, Inc. |
Chemical References |
- Cyclooxygenase Inhibitors
- Pyrazoles
- Sulfonamides
- Transcription Factor RelA
- Cyclooxygenase 2
- Celecoxib
|
Topics |
- Adenocarcinoma
(drug therapy, metabolism, pathology)
- Animals
- Apoptosis
(drug effects)
- Blotting, Western
- Celecoxib
- Cell Growth Processes
(drug effects)
- Cyclooxygenase 2
(metabolism)
- Cyclooxygenase Inhibitors
(pharmacology)
- Disease Models, Animal
- Dose-Response Relationship, Drug
- Down-Regulation
- Immunohistochemistry
- In Situ Nick-End Labeling
- Male
- Mice
- Mice, Inbred C57BL
- Mice, Transgenic
- Prostatic Intraepithelial Neoplasia
(drug therapy, metabolism, pathology)
- Prostatic Neoplasms
(drug therapy, metabolism, pathology)
- Pyrazoles
(pharmacology)
- Sulfonamides
(pharmacology)
- Transcription Factor RelA
(antagonists & inhibitors, biosynthesis)
|