| First Author | Roy HK | Year | 2005 |
| Journal | Cancer Lett | Volume | 217 |
| Issue | 2 | Pages | 161-9 |
| PubMed ID | 15617833 | Mgi Jnum | J:95217 |
| Mgi Id | MGI:3525714 | Doi | 10.1016/j.canlet.2004.07.042 |
| Citation | Roy HK, et al. (2005) The nonsteroidal anti-inflammatory drug, nabumetone, differentially inhibits beta-catenin signaling in the MIN mouse and azoxymethane-treated rat models of colon carcinogenesis. Cancer Lett 217(2):161-9 |
| abstractText | The mechanisms through which beta-catenin signaling is inhibited during colorectal cancer chemoprevention by nonsteroidal anti-inflammatory agents is incompletely understood. We report that nabumetone decreased uninvolved intestinal mucosal beta-catenin levels in the MIN mouse with a concomitant increase in glycogen synthase kinase (GSK)-3beta levels, an enzyme that targets beta-catenin for destruction. However, in the azoxymethane-treated rat, where beta-catenin is frequently rendered GSK-3beta-insensitive, nabumetone failed to alter beta-catenin levels but did decrease beta-catenin nuclear localization and transcriptional activity as gauged by cyclin D1. In conclusion, we demonstrate that the differential mechanisms for beta-catenin suppression may be determined, at least partly, by GSK-3beta. |
