Patterns of cyclooxygenase-1 and -2 expression in human gliomas in vivo

Deininger, Martin H.; Weller, Michael; Streffer, Johannes; Mittelbronn, Michel; Meyermann, Richard

doi:10.1007/s004010051075

Cited by 90 publications

(72 citation statements)

References 16 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…The expression of COX-2, as well as the levels of its reaction products, the prostaglandins, are frequently found elevated in gliomas. [39][40][41][42] In addition, high COX-2 expression is associated with clinically more aggressive tumors, e.g., glioblastoma multiforme, and is a strong predictor of poor survival. 43 It is therefore possible that the inhibition of COX-2 activity in such cells might be beneficial for the management of these tumors.…”

Section: Discussionmentioning

confidence: 99%

Differential Effects of Selective COX-2 Inhibitors on Cell Cycle Regulation and Proliferation of Glioblastoma Cell Lines

Kardosh¹,

Blumenthal²,

Wang³

et al. 2004

Cancer Biology & Therapy

View full text Add to dashboard Cite

B i o s c i e n c e . N o t f o r d i s t r i b u t i o n .[Cancer Biology & ACKNOWLEDGEMENTSWe are grateful to the following people for providing plasmids or cell lines: Frank B. Furnari, Webster K. Cavenee, William R. Taylor, and Toshio Nikaido. The technical assistance of Susan Su is acknowledged.This work was supported in part by the Kriegel Foundation (A.K.; T.C.C.). NOTE ADDED IN PROOFUsing prostate cancer cell lines, Johnson et al. (Adv Enzyme Regul 2001; 41:221-35) observed differential effects of selective COX-2 inhibitors on apoposis induction. Similar to our data presented here, they found celecoxib to be the most potent compound. Research Paper Differential Effects of Selective COX-2 Inhibitors on Cell Cycle Regulation and Proliferation of Glioblastoma Cell Lines ABSTRACTIt is well established that traditional NSAIDs, which inhibit cyclooxygenase (COX) 1 and COX-2, have the potential to reduce the risk of colorectal cancer. New generation COX inhibitors have been developed that selectively inhibit COX-2, which might cause less side effects while still retaining their therapeutic potential. As patients with brain tumors, such as glioblastoma, exhibit a very poor prognosis, we began to explore whether COX inhibitors could be useful for the treatment of this type of tumor. We found that celecoxib inhibited the proliferation of various glioblastoma cell lines in vitro much more potently than traditional NSAIDs. In addition, although several different selective COX-2 inhibitors potently reduced PGE2 levels in these cells, none of them exerted anti-proliferative effects that were comparable to celecoxib. The addition of external PGE2 to celecoxib-treated cells did not restore proliferation, indicating that growth inhibition by celecoxib was not mediated via the blockage of PGE2 production. In an effort to determine the underlying molecular processes that might mediate celecoxib's potent anti-proliferative effects, we found a loss of the activity of cyclin-dependent kinases, the essential regulators of cell proliferation, which was due to the transcriptional downregulation of cyclin A and cyclin B expression. Taken together, our results show that celecoxib exerts COX-2-independent anti-proliferative effects on glioblastoma cell growth, which are more potent than those of other selective COX-2 inhibitors or traditional NSAIDs, and which are mediated via the transcriptional inhibition of two essential components of the cell cycle machinery, cyclin A and cyclin B.

show abstract

Section: Discussionmentioning

confidence: 99%

Differential Effects of Selective COX-2 Inhibitors on Cell Cycle Regulation and Proliferation of Glioblastoma Cell Lines

Kardosh¹,

Blumenthal²,

Wang³

et al. 2004

Cancer Biology & Therapy

View full text Add to dashboard Cite

show abstract

“…6 COX-2 expression has also been detected in colorectal, gastric, esophageal, and lung carcinomas, as well as in brain tumors. [7][8][9][10][11][12][13] COX-2 has been reported to be important in the relationship between increased prostaglandin synthesis and the development of glioma and its progression.…”

Section: Introductionmentioning

confidence: 99%

Preparation of polylactide-co-glycolide nanoparticles incorporating celecoxib and their antitumor activity against brain tumor cells

Kim

Jeong²,

Jin³

et al. 2011

IJN

View full text Add to dashboard Cite

Background: Celecoxib, a cyclo-oxygenase (COX)-2 inhibitor, has been reported to mediate growth inhibitory effects and to induce apoptosis in various cancer cell lines. In this study, we examined the potential effects of celecoxib on glioma cell proliferation, migration, and inhibition of COX-2 expression in vitro. Methods: Celecoxib was incorporated into poly DL-lactide-co-glycolide (PLGA) nanoparticles for antitumor drug delivery. Results: PLGA nanoparticles incorporating celecoxib had spherical shapes and their particle sizes were in the range of 50-200 nm. Drug-loading efficiency was not significantly changed according to the solvent used, except for acetone. Celecoxib was released from the PLGA nanoparticles for more than 2 days, and the higher the drug content, the longer the duration of drug release. PLGA nanoparticles incorporating celecoxib showed cytotoxicity against U87MG tumor cells similar to that of celecoxib administered alone. Furthermore, celecoxib did not affect the degree of migration of U87MG cells. PLGA nanoparticles incorporating celecoxib showed dose-dependent cytotoxicity similar to that of celecoxib alone in C6 rat glioma cells. Western blot assay of the C6 cells showed that neither celecoxib alone nor PLGA nanoparticles incorporating celecoxib affected COX-2 expression. Conclusion: PLGA nanoparticles incorporating celecoxib had antitumor activity similar to that of celecoxib alone, even though these particles did not affect the degree of migration or COX-2 expression in the tumor cells.

show abstract

“…Cyclooxygenase (COX), an enzyme important for the synthesis of prostaglandins, is present in three isoforms. COX-1 shows low or constitutive expression in a variety of tissues (5,23,44) . COX-2 is highly inducible in response to cellular activation by hormones, proinflammatory cytokines, growth factors and tumor promoters (41,44) .…”

Section: Introductionmentioning

confidence: 99%

Evaluation of the immunoexpression of COX-1, COX-2 and p53 in Crohn's disease

Romero

Artigiani

Costa

et al. 2008

Arq. Gastroenterol.

View full text Add to dashboard Cite

-Background -Crohn's disease accompanied by nonspecific or idiopathic ulcerative proctocolitis corresponds to a condition called intestinal inflammatory disease. The immunoexpression of cyclooxygenase 2 (COX-2) in Crohn's disease becomes more marked with progression of the disease and the presence of wild-type p53 suppresses the transcription of COX-2. Aims -To investigate the immunoexpression of cyclooxygenase 1 (COX-1), COX-2 and p53 in Crohn's ileocolitis and to correlated this expression with clinical and histopathological parameters. Methods -Forty-five cases of Crohn's disease, 16 cases of actinic colitis (diseased-control group) and 11 cases without a history of intestinal disease (normal control group) were studied. Hematoxylin-eosin-stained sections were submitted to histopathological analysis and the immunohistochemical expression of COX-1, COX-2 and p53 was evaluated by the streptavidin-biotin-peroxidase method. Results -Sixty percent of the Crohn's disease patients were women and 40% were men, with 75.5% whites and 25.5% non-whites. The disease involved the terminal ileum in 44.5% of cases, ileum in 33.3%, colon in 20% and duodenum-ileum in 2.2%. A significant association was observed between COX-2 immunoreactivity and age ≤40 years. Histopathological analysis of Crohn's disease samples showed mild or moderate crypt distortion (57.8% and 35.6% of cases), atrophy (6.6%), mild, moderate and marked chronic inflammation (46.7%, 26.7% and 20%), acute inflammatory activity (93.3%), ulceration (24.4%), mucin depletion (37.8%), Paneth's cells (24.4%), intraepithelial lymphocytes (93.3%), and subepithelial collagen (6.7%). In the CD group, COX-1 immunoreactivity in epithelial and inflammatory cells was observed in 26.7% and 22.2% of cases, respectively.

show abstract

Patterns of cyclooxygenase-1 and -2 expression in human gliomas in vivo

Cited by 90 publications

References 16 publications

Differential Effects of Selective COX-2 Inhibitors on Cell Cycle Regulation and Proliferation of Glioblastoma Cell Lines

Differential Effects of Selective COX-2 Inhibitors on Cell Cycle Regulation and Proliferation of Glioblastoma Cell Lines

Preparation of polylactide-co-glycolide nanoparticles incorporating celecoxib and their antitumor activity against brain tumor cells

Evaluation of the immunoexpression of COX-1, COX-2 and p53 in Crohn's disease

Contact Info

Product

Resources

About