{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,17]],"date-time":"2026-02-17T23:05:33Z","timestamp":1771369533476,"version":"3.50.1"},"reference-count":42,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2005,8,5]],"date-time":"2005-08-05T00:00:00Z","timestamp":1123200000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["European J of Haematology"],"published-print":{"date-parts":[[2005,9]]},"abstract":"<jats:p><jats:bold>Abstract:\u2002<\/jats:bold> Cyclooxygenase\u20102 (COX\u20102) is reported to be an important cellular target for therapy in malignancies. The growth inhibitory effects of COX\u20102 inhibitors on malignancies have been demonstrated to be through not only COX\u20102 dependent, but also independent mechanisms. In this study, we showed that etodolac, COX\u20102 inhibitor, induced apoptosis via COX\u20102 independent pathway, and investigated the molecular details of etodolac\u2010induced apoptosis in Burkitt's lymphoma cells. In Daudi and Raji Burkitt's lymphoma cell lines, which expressed no COX\u20102 enzyme, etodolac more strongly induced apoptosis compared to meloxicam. Moreover, etodolac did not induce apoptosis to normal B\u2010lymphocytes. For the pathway of etodolac\u2010induced apoptosis, reduction of anti\u2010apoptotic <jats:italic>bcl\u20102<\/jats:italic> mRNA and Bcl\u20102 protein, activation of Caspase\u20109 and \u20103, down\u2010regulation of caspase inhibitors, c\u2010IAP\u20101 and Survivin were involved. Moreover, <jats:italic>EBER\u20101<\/jats:italic> and <jats:italic>\u20102<\/jats:italic> expression in Epstein\u2013Barr virus positive Daudi and Raji cells were reduced to result in down\u2010regulation of Bcl\u20102 by treatment with etodolac. It has been reported that etodolac has stereoisomers, R\u2010 and S\u2010etodolac. We found that racemate of etodolac more strongly induced apoptosis in Daudi and Raji cells compared to R\u2010 or S\u2010etodolac. In conclusion, our findings indicated etodolac inhibited <jats:italic>EBERs<\/jats:italic> expression and induced apoptosis via a Bcl\u20102\u2010regulated pathway. Moreover, racemate of etodolac more effectively induced apoptosis than R\u2010 and\/or S\u2010etodolac. Therefore, these activities of etodolac potentially extend to the treatment of patients with Burkitt's lymphoma resistant to chemotherapy.<\/jats:p>","DOI":"10.1111\/j.1600-0609.2005.00498.x","type":"journal-article","created":{"date-parts":[[2005,8,5]],"date-time":"2005-08-05T16:26:59Z","timestamp":1123259219000},"page":"212-220","source":"Crossref","is-referenced-by-count":26,"title":["Etodolac inhibits <i>EBER<\/i> expression and induces Bcl\u20102\u2010regulated apoptosis in Burkitt's lymphoma 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