Exploiting Cyclooxygenase-(in)dependent properties of COX-2 inhibitors for malignant glioma therapy

Anti-Cancer Agents in Medicinal Chemistry

Volumn 10, Issue 6, 2010, Pages 450-461

  Schönthal, Axel H ^a  

^a UNIVERSITY OF SOUTHERN CALIFORNIA   (United States)

Author keywords

Celecoxib; Cyclooxygenase; Dimethyl celecoxib; Glioblastoma; Glioma; NSAIDs; Rofecoxib; Valdecoxib

Indexed keywords

4 [5 (4 CHLOROPHENYL) 3 TRIFLUOROMETHYL 1H PYRAZOL 1 YL]BENZENESULFONAMIDE; ACETAZOLAMIDE; BEVACIZUMAB; BORTEZOMIB; CARBONATE DEHYDRATASE IX; CARBONATE DEHYDRATASE XII; CELECOXIB; DICLOFENAC; ETORICOXIB; FLURBIPROFEN; INDOMETACIN; IRINOTECAN; MELOXICAM; NIMESULIDE; PHOSPHOINOSITIDE DEPENDENT PROTEIN KINASE 1; ROFECOXIB; SULINDAC; TEMOZOLOMIDE; VALDECOXIB;

ANTIANGIOGENIC ACTIVITY; ANTINEOPLASTIC ACTIVITY; ARTICLE; CANCER CELL CULTURE; CANCER COMBINATION CHEMOTHERAPY; CANCER PATIENT; CANCER PREVENTION; CELL PROLIFERATION; CHEMOPROPHYLAXIS; CYTOTOXICITY; DRUG EFFICACY; ENDOPLASMIC RETICULUM STRESS; GLIOBLASTOMA; HUMAN; IN VITRO STUDY; IN VIVO STUDY; NONHUMAN; PROTEIN EXPRESSION; TUMOR RECURRENCE; TUMOR VOLUME;

EID: 78649890478     PISSN: 18715206     EISSN: None     Source Type: Journal    
DOI: 10.2174/1871520611009060450     Document Type: Article

References (178)

1. Khan, M.N.; Lee, Y.S. Cyclooxygenase inhibitors: Scope of theiruse and development in cancer chemotherapy. Med. Res. Rev., 2009, Dec 4, [Epub ahead of print].
2. Menter, D.G.; Schilsky, R.L.; Du Bois, R.N. Cyclooxygenase-2 and cancer treatment: understanding the risk should be worth thereward. Clin. Cancer Res., 2010, 16, 1384-1390.
3. Thun, M.J.; Henley, S.J.; Patrono, C. Nonsteroidal antiinflammatorydrugs as anticancer agents: mechanistic, pharmacologic, and clinical issues. J. Natl. Cancer Inst., 2002, 94, 252-266.
4. Hla, T.; Neilson, K. Human cyclooxygenase-2 cDNA. Proc. Natl.Acad. Sci. U S A, 1992, 89, 7384-7388.
5. Xie, W.L.; Chipman, J.G.; Robertson, D.L.; Erikson, R.L.; Simmons, D.L. Expression of a mitogen-responsive gene encodingprostaglandin synthase is regulated by mRNA splicing. Proc. Natl.Acad. Sci. U S A, 1991, 88, 2692-2696.
6. Fletcher, B.S.; Kujubu, D.A.; Perrin, D.M.; Herschman, H.R.Structure of the mitogen-inducible TIS10 gene and demonstrationthat the TIS10-encoded protein is a functional prostaglandin G/Hsynthase. J. Biol. Chem., 1992, 267, 4338-4344.
7. Legler, D.F.; Bruckner, M.; Uetz-von Allmen, E.; Krause, P.Prostaglandin E2 at new glance: novel insights in functionaldiversity of fer therapeutic chances. Int. J. Biochem. Cell Biol., 42, 198-201.
8. Smith, W.L.; De Witt, D.L.; Garavito, R.M. Cyclooxygenases: structural, cellular, and molecular biology. Annu. Rev. Biochem., 2000, 69, 145-182.
9. Vane, J.R.; Bakhle, Y.S.; Botting, R.M. Cyclooxygenases 1 and 2.Annu. Rev. Pharmacol. Toxicol., 1998, 38, 97-120.
10. Hawk, E.T.; Viner, J.L.; Dannenberg, A.; Du Bois, R.N. COX-2 incancer--a player that's defining the rules. J. Natl. Cancer Inst., 2002, 94, 545-546.
11. Subbaramaiah, K.; Telang, N.; Ramonetti, J.T.; Araki, R.; De Vito, B.; Weksler, B.B.; Dannenberg, A.J. Transcription of cyclooxygenase-2 is enhanced in transformed mammary epithelialcells. Cancer Res., 1996, 56, 4424-4429.
12. Tsuji, S.; Tsujii, M.; Kawano, S.; Hori, M. Cyclooxygenase-2upregulation as a perigenetic change in carcinogenesis. J. Exp.Clin. Cancer Res., 2001, 20, 117-129.
13. Rao, C.V.; Reddy, B.S. NSAIDs and chemoprevention. Curr.Cancer Drug Targets, 2004, 4, 29-42.
14. Thun, M.J.; Namboodiri, M.M.; Heath, C.W., Jr. Aspirin use and reduced risk of fatal colon cancer. N. Engl. J. Med., 1991, 325, 1593-1596.
15. Davies, N.M.; Reynolds, J.K.; Undeberg, M.R.; Gates, B.J.; Ohgami, Y.; Vega-Villa, K.R. Minimizing risks of NSAIDs: cardiovascular, gastrointestinal and renal. Expert Rev. Neurother., 2006, 6, 1643-1655.
16. Laine, L. GI risk and risk factors of NSAIDs. J. Cardiovasc.Pharmacol., 2006, 47 Suppl 1, S60-66.
17. Arber, N.; Eagle, C.J.; Spicak, J.; Racz, I.; Dite, P.; Hajer, J.; Zavoral, M.; Lechuga, M.J.; Gerletti, P.; Tang, J.; Rosenstein, R.B.; Macdonald, K.; Bhadra, P.; Fowler, R.; Wittes, J.; Zauber, A.G.; Solomon, S.D.; Levin, B. Celecoxib for the prevention of colorectaladenomatous polyps. N. Engl. J. Med., 2006, 355, 885-895.
18. Bertagnolli, M.M.; Eagle, C.J.; Zauber, A.G.; Redston, M.; Solomon, S.D.; Kim, K.; Tang, J.; Rosenstein, R.B.; Wittes, J.; Corle, D.; Hess, T.M.; Woloj, G.M.; Boisserie, F.; Anderson, W.F.; Viner, J.L.; Bagheri, D.; Burn, J.; Chung, D.C.; Dewar, T.; Foley, T.R.; Hoffman, N.; Macrae, F.; Pruitt, R.E.; Saltzman, J.R.; Salzberg, B.; Sylwestrowicz, T.; Gordon, G.B.; Hawk, E.T.Celecoxib for the prevention of sporadic colorectal adenomas. N.Engl. J. Med., 2006, 355, 873-884.
19. Bresalier, R.S.; Sandler, R.S.; Quan, H.; Bolognese, J.A.; Oxenius, B.; Horgan, K.; Lines, C.; Riddell, R.; Morton, D.; Lanas, A.; Konstam, M.A.; Baron, J.A. Cardiovascular events associated withrofecoxib in a colorectal adenoma chemoprevention trial. N. Engl.J. Med., 2005, 352, 1092-1102.
20. Baron, J.A.; Sandler, R.S.; Bresalier, R.S.; Lanas, A.; Morton, D.G.; Riddell, R.; Iverson, E.R.; Demets, D.L. Cardiovascularevents associated with rofecoxib: final analysis of the APPROVetrial. Lancet, 2008, 372, 1756-1764.
21. Ray, W.A.; Griffin, M.R.; Stein, C.M. Cardiovascular toxicity of valdecoxib. N. Engl. J. Med., 2004, 351, 2767.
22. Matsumoto, A.K.; Cavanaugh, P.F., Jr. Etoricoxib. Drugs Today(Barc), 2004, 40, 395-414.
23. Barden, J.; Edwards, J.E.; McQuay, H.J.; Moore, R.A. Oralvaldecoxib and injected parecoxib for acute postoperative pain: aquantitative systematic review. BMC Anesthesiol., 2003, 3, 1.
24. Mysler, E. Lumiracoxib (Prexige): a new selective COX-2inhibitor. Int. J. Clin. Pract., 2004, 58, 606-611.
25. Brophy, J.M. Cardiovascular effects of cyclooxygenase-2inhibitors. Curr. Opin. Gastroenterol., 2007, 23, 617-624.
26. Dajani, E.Z.; Islam, K. Cardiovascular and gastrointestinal toxicityof selective cyclo-oxygenase-2 inhibitors in man. J. Physiol.Pharmacol., 2008, 59 Suppl 2, 117-133.
27. Sanghi, S.; MacLaughlin, E.J.; Jewell, C.W.; Chaffer, S.; Naus, P.J.; Watson, L.E.; Dostal, D.E. Cyclooxygenase-2 inhibitors: apainful lesson. Cardiovasc. Hematol. Disord. Drug Targets, 2006, 6, 85-100.
28. Dannenberg, A.J.; Subbaramaiah, K. Targeting cyclooxygenase-2in human neoplasia: rationale and promise. Cancer Cell, 2003, 4, 431-436.
29. Keller, J.J.; Giardiello, F.M. Chemoprevention strategies usingNSAIDs and COX-2 inhibitors. Cancer Biol. Ther., 2003, 2, S140-149.
30. Marnett, L.J.; Kalgutkar, A.S. Cyclooxygenase 2 inhibitors: discovery, selectivity and the future. Trends Pharmacol. Sci., 1999, 20, 465-469.
31. Bradley, C.P. Review: risk for cardiovascular events is increasedwith rofecoxib, diclofenac, and indomethacin but not celecoxib.ACP J. Club, 2007, 146, 24.
32. McGettigan, P.; Henry, D. Cardiovascular risk and inhibition of cyclooxygenase: a systematic review of the observational studies of selective and nonselective inhibitors of cyclooxygenase 2. JAMA, 2006, 296, 1633-1644.
33. Gudbjornsson, B.; Thorsteinsson, S.B.; Sigvaldason, H.; Einarsdottir, R.; Johannsson, M.; Zoega, H.; Halldorsson, M.; Thorgeirsson, G. Rofecoxib, but not celecoxib, increases the risk of thromboembolic cardiovascular events in young adults-anationwide registry-based study. Eur. J. Clin. Pharmacol., 2010, 66, 619-625.
34. Solomon, S.D.; Wittes, J.; Finn, P.V.; Fowler, R.; Viner, J.; Bertagnolli, M.M.; Arber, N.; Levin, B.; Meinert, C.L.; Martin, B.; Pater, J.L.; Goss, P.E.; Lance, P.; Obara, S.; Chew, E.Y.; Kim, J.; Arndt, G.; Hawk, E. Cardiovascular risk of celecoxib in 6randomized placebo-controlled trials: the cross trial safety analysis.Circulation, 2008, 117, 2104-2113.
35. FitzGerald, G.A.; Patrono, C. The coxibs, selective inhibitors of cyclooxygenase-2. N. Engl. J. Med., 2001, 345, 433-442.
36. Bennett, A.; Tavares, I.A. COX-2 inhibitors compared and contrasted. Expert Opin. Pharmacother., 2001, 2, 1859-1876.
37. Capone, M.L.; Tacconelli, S.; Di Francesco, L.; Sacchetti, A.; Sciulli, M.G.; Patrignani, P. Pharmacodynamic of cyclooxygenaseinhibitors in humans. Prostaglandins Other Lipid Mediat., 2007, 82, 85-94.
38. Bjarnason, I.; Thjodleifsson, B. The murky world of the COX-2-selective agents. Inflammopharmacology, 2005, 13, 381-393.
39. Khasraw, M.; Lassman, A.B. Advances in the treatment of malignant gliomas. Curr. Oncol. Rep., 2010, 12, 26-33.
40. Quick, A.; Patel, D.; Hadziahmetovic, M.; Chakravarti, A.; Mehta, M. Current therapeutic paradigms in glioblastoma. Rev. RecentClin. Trials, 2010, 5, 14-27.
41. Lin, C.L.; Lieu, A.S.; Lee, K.S.; Yang, Y.H.; Kuo, T.H.; Hung, M.H.; Loh, J.K.; Yen, C.P.; Chang, C.Z.; Howng, S.L.; Hwang, S.L. The conditional probabilities of survival in patients withanaplastic astrocytoma or glioblastoma multiforme. Surg. Neurol., 2003, 60, 402-406.
42. Krex, D.; Klink, B.; Hartmann, C.; von Deimling, A.; Pietsch, T.; Simon, M.; Sabel, M.; Steinbach, J.P.; Heese, O.; Reifenberger, G.; Weller, M.; Schackert, G. Long-term survival with glioblastomamultiforme. Brain, 2007, 130, 2596-2606.
43. Affronti, M.L.; Heery, C.R.; Herndon, J.E., 2nd; Rich, J.N.; Reardon, D.A.; Desjardins, A.; Vredenburgh, J.J.; Friedman, A.H.; Bigner, D.D.; Friedman, H.S. Overall survival of newly diagnosedglioblastoma patients receiving carmustine wafers followed byradiation and concurrent temozolomide plus rotational multiagentchemotherapy. Cancer, 2009, 115, 3501-3511.
44. Villavicencio, A.T.; Burneikiene, S.; Romanelli, P.; Fariselli, L.; McNeely, L.; Lipani, J.D.; Chang, S.D.; Nelson, E.L.; McIntyre, M.; Broggi, G.; Adler, J.R., Jr. Survival following stereotacticradiosurgery for newly diagnosed and recurrent glioblastomamultiforme: a multicenter experience. Neurosurg. Rev., 2009, 32, 417-424.
45. Zhang, M.; Chakravarti, A. Novel radiation-enhancing agents inmalignant gliomas. Semin. Radiat Oncol., 2006, 16, 29-37.
46. Okuda, T.; Kataoka, K.; Yabuuchi, T.; Yugami, H.; Kato, A.Fluorescence-guided surgery of metastatic brain tumors usingfluorescein sodium. J. Clin. Neurosci., 2010, 17, 118-121.
47. Norden, A.D.; Drappatz, J.; Wen, P.Y. Antiangiogenic therapies forhigh-grade glioma. Nat. Rev. Neurol., 2009, 5, 610-620.
48. Verhoeff, J.J.; van Tellingen, O.; Claes, A.; Stalpers, L.J.; van Linde, M.E.; Richel, D.J.; Leenders, W.P.; van Furth, W.R.Concerns about anti-angiogenic treatment in patients withglioblastoma multiforme. BMC Cancer, 2009, 9, 444.
49. Engblom, D.; Ek, M.; Saha, S.; Ericsson-Dahlstrand, A.; Jakobsson, P.J.; Blomqvist, A. Prostaglandins as inflammatorymessengers across the blood-brain barrier. J. Mol. Med., 2002, 80, 5-15.
50. Siesjo, B.K.; Nilsson, B. Prostaglandins and the cerebralcirculation. Adv Prostaglandin Thromboxane Leukot. Res., 1982, 10, 367-380.
51. Castelli, M.G.; Butti, G.; Chiabrando, C.; Cozzi, E.; Fanelli, R.; Gaetani, P.; Silvani, V.; Paoletti, P. Arachidonic acid metabolicprofiles in human meningiomas and gliomas. J. Neurooncol., 1987, 5, 369-375.
52. Castelli, M.G.; Chiabrando, C.; Fanelli, R.; Martelli, L.; Butti, G.; Gaetani, P.; Paoletti, P. Prostaglandin and thromboxane synthesisby human intracranial tumors. Cancer Res., 1989, 49, 1505-1508.
53. Paoletti, P.; Chiabrando, C.; Gaetani, P.; Castelli, M.G.; Butti, G.; Martelli, L.; Rolli, M. Prostaglandins in human brain tumors. J.Neurosurg. Sci., 1989, 33, 65-69.
54. Kokoglu, E.; Tuter, Y.; Sandikci, K.S.; Yazici, Z.; Ulakoglu, E.Z.; Sonmez, H.; Ozyurt, E. Prostaglandin E2 levels in human braintumor tissues and arachidonic acid levels in the plasma membraneof human brain tumors. Cancer Lett., 1998, 132, 17-21.
55. Mattila, S.; Tuominen, H.; Koivukangas, J.; Stenback, F. Theterminal prostaglandin synthases mPGES-1, mPGES-2, and cPGESare all overexpressed in human gliomas. Neuropathology, 2009, 29, 156-165.
56. Deininger, M.H.; Weller, M.; Streffer, J.; Mittelbronn, M.; Meyermann, R. Patterns of cyclooxygenase-1 and -2 expression inhuman gliomas in vivo. Acta Neuropathol. (Berl), 1999, 98, 240-244.
57. Joki, T.; Heese, O.; Nikas, D.C.; Bello, L.; Zhang, J.; Kraeft, S.K.; Seyfried, N.T.; Abe, T.; Chen, L.B.; Carroll, R.S.; Black, P.M.Expression of cyclooxygenase 2 (COX-2) in human glioma and invitro inhibition by a specific COX-2 inhibitor, NS-398. CancerRes., 2000, 60, 4926-4931.
58. Prayson, R.A.; Castilla, E.A.; Vogelbaum, M.A.; Barnett, G.H.Cyclooxygenase-2 (COX-2) expression by immunohistochemistryin glioblastoma multiforme. Ann. Diagn. Pathol., 2002, 6, 148-153.
59. Shono, T.; Tofilon, P.J.; Bruner, J.M.; Owolabi, O.; Lang, F.F.Cyclooxygenase-2 expression in human gliomas: prognosticsignificance and molecular correlations. Cancer Res., 2001, 61, 4375-4381.
60. Choy, H.; Milas, L. Enhancing radiotherapy with cyclooxygenase-2enzyme inhibitors: a rational advance? J. Natl. Cancer Inst., 2003, 95, 1440-1452.
61. Milas, L.; Mason, K.A.; Crane, C.H.; Liao, Z.; Masferrer, J.Improvement of radiotherapy or chemoradiotherapy by targetingCOX-2 enzyme. Oncology (Huntingt), 2003, 17, 15-24.
62. Petersen, C.; Petersen, S.; Milas, L.; Lang, F.F.; Tofilon, P.J.Enhancement of intrinsic tumor cell radiosensitivity induced by aselective cyclooxygenase-2 inhibitor. Clin. Cancer Res., 2000, 6, 2513-2520.
63. Casper, D.; Lekhraj, R.; Yaparpalvi, U.S.; Pidel, A.; Jaggernauth, W.A.; Werner, P.; Tribius, S.; Rowe, J.D.; La Sala, P.A.Acetaminophen selectively reduces glioma cell growth and increases radiosensitivity in culture. J. Neurooncol., 2000, 46, 215-229.
64. Bijnsdorp, I.V.; van den Berg, J.; Kuipers, G.K.; Wedekind, L.E.; Slotman, B.J.; van Rijn, J.; Lafleur, M.V.; Sminia, P.Radiosensitizing potential of the selective cyclooygenase-2 (COX-2) inhibitor meloxicam on human glioma cells. J. Neurooncol., 2007, 85, 25-31.
65. Kuipers, G.K.; Slotman, B.J.; Wedekind, L.E.; Stoter, T.R.; Berg, J.; Sminia, P.; Lafleur, M.V. Radiosensitization of human gliomacells by cyclooxygenase-2 (COX-2) inhibition: independent onCOX-2 expression and dependent on the COX-2 inhibitor and sequence of administration. Int. J. Radiat. Biol., 2007, 83, 677-685.
66. Kang, K.B.; Wang, T.T.; Woon, C.T.; Cheah, E.S.; Moore, X.L.; Zhu, C.; Wong, M.C. Enhancement of glioblastoma radioresponseby a selective COX-2 inhibitor celecoxib: inhibition of tumorangiogenesis with extensive tumor necrosis. Int. J. Radiat. Oncol.Biol. Phys., 2007, 67, 888-896.
67. Wagemakers, M.; van der Wal, G.E.; Cuberes, R.; Alvarez, I.; Andres, E.M.; Buxens, J.; Vela, J.M.; Moorlag, H.; Mooij, J.J.; Molema, G. COX-2 inhibition combined with radiation reducesorthotopic glioma outgrowth by targeting the tumor vasculature.Transl. Oncol., 2009, 2, 1-7.
68. Cerchietti, L.C.; Bonomi, M.R.; Navigante, A.H.; Castro, M.A.; Cabalar, M.E.; Roth, B.M. Phase I/II study of selectivecyclooxygenase-2 inhibitor celecoxib as a radiation sensitizer inpatients with unresectable brain metastases. J. Neurooncol., 2005, 71, 73-81.
69. Gately, S.; Li, W.W. Multiple roles of COX-2 in tumorangiogenesis: a target for antiangiogenic therapy. Semin. Oncol., 2004, 31, 2-11.
70. Davis, T.W.; O'Neal, J.M.; Pagel, M.D.; Zweifel, B.S.; Mehta, P.P.; Heuvelman, D.M.; Masferrer, J.L. Synergy between celecoxiband radiotherapy results from inhibition of cyclooxygenase-2-derived prostaglandin E2, a survival factor for tumor and associatedvasculature. Cancer Res., 2004, 64, 279-285.
71. Leahy, K.M.; Ornberg, R.L.; Wang, Y.; Zweifel, B.S.; Koki, A.T.; Masferrer, J.L. Cyclooxygenase-2 inhibition by celecoxib reducesproliferation and induces apoptosis in angiogenic endothelial cellsin vivo. Cancer Res., 2002, 62, 625-631.
72. Williams, C.S.; Tsujii, M.; Reese, J.; Dey, S.K.; Du Bois, R.N. Hostcyclooxygenase-2 modulates carcinoma growth. J. Clin. Invest., 2000, 105, 1589-1594.
73. Toomey, D.P.; Murphy, J.F.; Conlon, K.C. COX-2, VEGF and tumour angiogenesis. Surgeon, 2009, 7, 174-180.
74. Eberhard, A.; Kahlert, S.; Goede, V.; Hemmerlein, B.; Plate, K.H.; Augustin, H.G. Heterogeneity of angiogenesis and blood vesselmaturation in human tumors: implications for antiangiogenic tumortherapies. Cancer Res., 2000, 60, 1388-1393.
75. Kunkel, P.; Ulbricht, U.; Bohlen, P.; Brockmann, M.A.; Fillbrandt, R.; Stavrou, D.; Westphal, M.; Lamszus, K. Inhibition of gliomaangiogenesis and growth in vivo by systemic treatment with amonoclonal antibody against vascular endothelial growth factorreceptor-2. Cancer Res., 2001, 61, 6624-6628.
76. Lamszus, K.; Brockmann, M.A.; Eckerich, C.; Bohlen, P.; May, C.; Mangold, U.; Fillbrandt, R.; Westphal, M. Inhibition of glioblastoma angiogenesis and invasion by combined treatmentsdirected against vascular endothelial growth factor receptor-2, epidermal growth factor receptor, and vascular endothelialcadherin.Clin. Cancer Res., 2005, 11, 4934-4940.
77. Paez-Ribes, M.; Allen, E.; Hudock, J.; Takeda, T.; Okuyama, H.; Vinals, F.; Inoue, M.; Bergers, G.; Hanahan, D.; Casanovas, O.Antiangiogenic therapy elicits malignant progression of tumors toincreased local invasion and distant metastasis. Cancer Cell, 2009, 15, 220-231.
78. Tuettenberg, J.; Grobholz, R.; Seiz, M.; Brockmann, M.A.; Lohr, F.; Wenz, F.; Vajkoczy, P. Recurrence pattern in glioblastomamultiforme patients treated with anti-angiogenic chemotherapy. J.Cancer Res. Clin. Oncol., 2009, 135, 1239-1244.
79. Wick, W.; Weller, M.; van den Bent, M.; Stupp, R. Bevacizumaband recurrent malignant gliomas: a European perspective. J. Clin.Oncol., 2010, 28, e188-189; author reply e190-182.
80. Seiz, M.; Nolte, I.; Pechlivanis, I.; Freyschlag, C.F.; Schmieder, K.; Vajkoczy, P.; Tuettenberg, J. Far-distant metastases along the CSFpathway of glioblastoma multiforme during continuous low-dosechemotherapy with temozolomide and celecoxib. Neurosurg. Rev., 2010, 33, 375-381.
81. Reardon, D.A.; Quinn, J.A.; Vredenburgh, J.; Rich, J.N.; Gururangan, S.; Badruddoja, M.; Herndon, J.E., 2nd; Dowell, J.M.; Friedman, A.H.; Friedman, H.S. Phase II trial of irinotecan pluscelecoxib in adults with recurrent malignant glioma. Cancer, 2005, 103, 329-338.
82. Levin, V.A.; Giglio, P.; Puduvalli, V.K.; Jochec, J.; Groves, M.D.; Yung, W.K.; Hess, K. Combination chemotherapy with 13-cisretinoicacid and celecoxib in the treatment of glioblastomamultiforme. J. Neurooncol., 2006, 78, 85-90.
83. Stockhammer, F.; Misch, M.; Koch, A.; Czabanka, M.; Plotkin, M.; Blechschmidt, C.; Tuettenberg, J.; Vajkoczy, P. Continuous lowdosetemozolomide and celecoxib in recurrent glioblastoma. J Neurooncol, 2010, May 6 [Epub ahead of print].
84. Kesari, S.; Schiff, D.; Henson, J.W.; Muzikansky, A.; Gigas, D.C.; Doherty, L.; Batchelor, T.T.; Longtine, J.A.; Ligon, K.L.; Weaver, S.; Laforme, A.; Ramakrishna, N.; Black, P.M.; Drappatz, J.; Ciampa, A.; Folkman, J.; Kieran, M.; Wen, P.Y. Phase II study of temozolomide, thalidomide, and celecoxib for newly diagnosedglioblastoma in adults. Neuro Oncol., 2008, 10, 300-308.
85. Walbert, T.; Gilbert, M.R.; Groves, M.D.; Puduvalli, V.K.; AlfredYung, W.K.; Conrad, C.A.; Bobustuc, G.C.; Colman, H.; Hsu, S.H.; Nebiyou Bekele, B.; Qiao, W.; Levin, V.A. Combination of6-thioguanine, capecitabine, and celecoxib with temozolomide orlomustine for recurrent high-grade glioma. J. Neurooncol., 2010, Jul 23 [Epub ahead of print].
86. Hau, P.; Kunz-Schughart, L.; Bogdahn, U.; Baumgart, U.; Hirschmann, B.; Weimann, E.; Muhleisen, H.; Ruemmele, P.; Steinbrecher, A.; Reichle, A. Low-dose chemotherapy incombination with COX-2 inhibitors and PPAR-gamma agonists inrecurrent high-grade gliomas - a phase II study. Oncology, 2007, 73, 21-25.
87. Buecher, B.; Bouancheau, D.; Broquet, A.; Bezieau, S.; Denis, M.G.; Bonnet, C.; Heymann, M.F.; Jarry, A.; Galmiche, J.P.; Blottiere, H.M. Growth inhibitory effect of celecoxib and rofecoxibon human colorectal carcinoma cell lines. Anticancer Res, 2005, 25(1A), 225-233.
88. Kardosh, A.; Blumenthal, M.; Wang, W.J.; Chen, T.C.; Schönthal, A.H. Differential effects of selective COX-2 inhibitors on cellcycle regulation and proliferation of glioblastoma cell lines. CancerBiol. Ther., 2004, 3, 9-16.
89. Niederberger, E.; Manderscheid, C.; Grosch, S.; Schmidt, H.; Ehnert, C.; Geisslinger, G. Effects of the selective COX-2inhibitors celecoxib and rofecoxib on human vascular cells.Biochem. Pharmacol., 2004, 68, 341-350.
90. Patel, M.I.; Subbaramaiah, K.; Du, B.; Chang, M.; Yang, P.; Newman, R.A.; Cordon-Cardo, C.; Thaler, H.T.; Dannenberg, A.J.Celecoxib inhibits prostate cancer growth: Evidence of acyclooxygenase-2-independent mechanism. Clin. Cancer Res., 2005, 11, 1999-2007.
91. Yamazaki, R.; Kusunoki, N.; Matsuzaki, T.; Hashimoto, S.; Kawai, S. Selective cyclooxygenase-2 inhibitors show a differential abilityto inhibit proliferation and induce apoptosis of colonadenocarcinoma cells. FEBS Lett., 2002, 531, 278-284.
92. Grösch, S.; Tegeder, I.; Niederberger, E.; Bräutigam, L.; Geisslinger, G. COX-2 independent induction of cell cycle arrestand apoptosis in colon cancer cells by the selective COX-2inhibitor celecoxib. FASEB J., 2001, 15, 2742-2744.
93. Lev-Ari, S.; Kazanov, D.; Liberman, E.; Ben-Yosef, R.; Arber, N.Down-regulation of PGE2 by physiologic levels of celecoxib is notsufficient to induce apoptosis or inhibit cell proliferation in humancolon carcinoma cell lines. Dig. Dis. Sci., 2007, 52, 1128-1133.
94. Schiffmann, S.; Maier, T.J.; Wobst, I.; Janssen, A.; Corban-Wilhelm, H.; Angioni, C.; Geisslinger, G.; Grosch, S. The antiproliferativepotency of celecoxib is not a class effect of coxibs.Biochem. Pharmacol., 2008, 76, 179-187.
95. Sun, S.Y.; Schroeder, C.P.; Yue, P.; Lotan, D.; Hong, W.K.; Lotan, R. Enhanced Growth Inhibition and Apoptosis Induction inNSCLC Cell Lines by Combination of Celecoxib and 4HPR atClinically Relevant Concentrations. Cancer Biol. Ther., 2005, 4, 407-413.
96. Waskewich, C.; Blumenthal, R.D.; Li, H.; Stein, R.; Goldenberg, D.M.; Burton, J. Celecoxib exhibits the greatest potency amongstcyclooxygenase (COX) inhibitors for growth inhibition of COX-2-negative hematopoietic and epithelial cell lines. Cancer Res., 2002, 62, 2029-2033.
97. Zhang, X.; Morham, S.G.; Langenbach, R.; Young, D.A. Malignanttransformation and antineoplastic actions of nonsteroidalantiinflammatory drugs (NSAIDs) on cyclooxygenase-null embryofibroblasts. J. Exp. Med., 1999, 190, 451-459.
98. Kulp, S.K.; Yang, Y.T.; Hung, C.C.; Chen, K.F.; Lai, J.P.; Tseng, P.H.; Fowble, J.W.; Ward, P.J.; Chen, C.S. 3-phosphoinositidedependentprotein kinase-1/Akt signaling represents a majorcyclooxygenase-2-independent target for celecoxib in prostatecancer cells. Cancer Res., 2004, 64, 1444-1451.
99. Pyrko, P.; Kardosh, A.; Liu, Y.T.; Soriano, N.; Xiong, W.; Chow, R.H.; Uddin, J.; Petasis, N.A.; Mircheff, A.K.; Farley, R.A.; Louie, S.G.; Chen, T.C.; Schönthal, A.H. Calcium-activated ER stress as amajor component of tumor cell death induced by 2, 5-dimethylcelecoxib(DMC), a non-coxib analog of celecoxib. Mol. CancerTher., 2007, 6, 1262-1275.
100. Paulson, S.K.; Kaprak, T.A.; Gresk, C.J.; Fast, D.M.; Baratta, M.T.; Burton, E.G.; Breau, A.P.; Karim, A. Plasma protein bindingof celecoxib in mice, rat, rabbit, dog and human. Biopharm. DrugDispos., 1999, 20, 293-299.
101. Kardosh, A.; Wang, W.; Uddin, J.; Petasis, N.A.; Hofman, F.; Chen, C.C.; Schönthal, A.H. Dimethyl-celecoxib (DMC), aderivative of celecoxib that lacks cyclooxygenase-2-inhibitoryfunction, potently mimics the anti-tumor effects of celecoxib onBurkitt's lymphoma in vitro and in vivo. Cancer Biol. Ther., 2005, 4, 571-582.
102. Masferrer, J.L.; Leahy, K.M.; Koki, A.T.; Zweifel, B.S.; Settle, S.L.; Woerner, B.M.; Edwards, D.A.; Flickinger, A.G.; Moore, R.J.; Seibert, K. Antiangiogenic and antitumor activities of cyclooxygenase-2 inhibitors. Cancer Res., 2000, 60, 1306-1311.
103. Trifan, O.C.; Durham, W.F.; Salazar, V.S.; Horton, J.; Levine, B.D.; Zweifel, B.S.; Davis, T.W.; Masferrer, J.L. Cyclooxygenase-2 inhibition with celecoxib enhances antitumor efficacy and reduces diarrhea side effect of CPT-11. Cancer Res., 2002, 62, 5778-5784.
104. Williams, C.S.; Watson, A.J.; Sheng, H.; Helou, R.; Shao, J.; Du Bois, R.N. Celecoxib prevents tumor growth in vivo withouttoxicity to normal gut: lack of correlation between in vitro and invivo models. Cancer Res., 2000, 60, 6045-6051.
105. Zweifel, B.S.; Davis, T.W.; Ornberg, R.L.; Masferrer, J.L. Directevidence for a role of cyclooxygenase 2-derived prostaglandin E2in human head and neck xenograft tumors. Cancer Res., 2002, 62, 6706-6711.
106. Kawamori, T.; Rao, C.V.; Seibert, K.; Reddy, B.S.Chemopreventive activity of celecoxib, a specific cyclooxygenase-2 inhibitor, against colon carcinogenesis. Cancer Res., 1998, 58, 409-412.
107. Drazen, J.M. COX-2 inhibitors--a lesson in unexpected problems.N. Engl. J. Med., 2005, 352, 1131-1132.
108. Fosslien, E. Cardiovascular complications of non-steroidal antiinflammatorydrugs. Ann. Clin. Lab. Sci., 2005, 35, 347-385.
109. Penning, T.D.; Talley, J.J.; Bertenshaw, S.R.; Carter, J.S.; Collins, P.W.; Docter, S.; Graneto, M.J.; Lee, L.F.; Malecha, J.W.; Miyashiro, J.M.; Rogers, R.S.; Rogier, D.J.; Yu, S.S.; AndersonGd; Burton, E.G.; Cogburn, J.N.; Gregory, S.A.; Koboldt, C.M.; Perkins, W.E.; Seibert, K.; Veenhuizen, A.W.; Zhang, Y.Y.; Isakson, P.C. Synthesis and biological evaluation of the 1, 5-diarylpyrazole class of cyclooxygenase-2 inhibitors: identificationof 4-[5-(4-methylphenyl)-3-(trifluoromethyl)-1H-pyrazol-1-yl]benze nesulfonamide (SC-58635, celecoxib). J. Med. Chem., 1997, 40, 1347-1365.
110. Song, X.; Lin, H.P.; Johnson, A.J.; Tseng, P.H.; Yang, Y.T.; Kulp, S.K.; Chen, C.S. Cyclooxygenase-2, player or spectator incyclooxygenase-2 inhibitor-induced apoptosis in prostate cancercells. J. Natl. Cancer Inst., 2002, 94, 585-591.
111. Zhu, J.; Song, X.; Lin, H.P.; Young, D.C.; Yan, S.; Marquez, V.E.; Chen, C.S. Using cyclooxygenase-2 inhibitors as molecularplatforms to develop a new class of apoptosis-inducing agents. J.Natl. Cancer Inst., 2002, 94, 1745-1757.
112. Chuang, H.-C.; Kardosh, A.; Gaffney, K.J.; Petasis, N.A.; Schönthal, A.H. COX-2 inhibition is neither necessary norsufficient for celecoxib to suppress tumor cell proliferation and focus formation in vitro. Mol. Cancer, 2008, 7, 38.
113. Kardosh, A.; Soriano, N.; Liu, Y.-T.; Uddin, J.; Petasis, N.A.; Hofman, F.; Chen, C.C.; Schönthal, A.H. Multi-target inhibition of drug-resistant multiple myeloma cell lines by dimethyl-celecoxib(DMC), a non-COX-2-inhibitory analog of celecoxib. Blood, 2005, 106, 4330-4338.
114. Yacoub, A.; Park, M.A.; Hanna, D.; Hong, Y.; Mitchell, C.; Pandya, A.P.; Harada, H.; Powis, G.; Chen, C.S.; Koumenis, C.; Grant, S.; Dent, P. OSU-03012 promotes caspase-independent butPERK-, cathepsin B-, BID-, and AIF-dependent killing of transformed cells. Mol. Pharmacol., 2006, 70, 589-603.
115. Flower, R.J. The development of COX2 inhibitors. Nat. Rev. DrugDiscov., 2003, 2, 179-191.
116. Pouplana, R.; Lozano, J.J.; Perez, C.; Ruiz, J. Structure-basedQSAR study on differential inhibition of human prostaglandinendoperoxide H synthase-2 (COX-2) by nonsteroidal antiinflammatorydrugs. J. Comput. Aided Mol. Des., 2002, 16, 683-709.
117. Schönthal, A.H. Induction of apoptosis by celecoxib in cell culture: an uncertain role for COX-2. Cancer Res., 2007, 67, 5575-5576.
118. Pyrko, P.; Soriano, N.; Kardosh, A.; Liu, Y.T.; Uddin, J.; Petasis, N.A.; Hofman, F.M.; Chen, C.S.; Chen, T.C.; Schönthal, A.H.Downregulation of survivin expression and concomitant inductionof apoptosis by celecoxib and its non-cyclooxygenase-2-inhibitoryanalog, dimethyl-celecoxib (DMC), in tumor cells in vitro and in vivo. Mol. Cancer, 2006, 5, 19.
119. Kardosh, A.; Golden, E.B.; Pyrko, P.; Uddin, J.; Hofman, F.M.; Chen, T.C.; Louie, S.G.; Petasis, N.A.; Schonthal, A.H. Aggravatedendoplasmic reticulum stress as a basis for enhanced glioblastomacell killing by bortezomib in combination with celecoxib or its noncoxibanalogue, 2, 5-dimethyl-celecoxib. Cancer Res., 2008, 68, 843-851.
120. Virrey, J.J.; Kardosh, A.; Golden, E.G.; Louie, S.G.; Petasis, N.A.; Schönthal, A.H.; Chen, T.C.; Hofman, F.M. Antiangiogenicactivities of 2, 5-dimethyl-celecoxib on the tumor vasculature. Mol.Cancer Ther., 2010, 9, 631-641.
121. Lin, H.P.; Kulp, S.K.; Tseng, P.H.; Yang, Y.T.; Yang, C.C.; Chen, C.S.; Chen, C.S. Growth inhibitory effects of celecoxib in humanumbilical vein endothelial cells are mediated through G1 arrest viamultiple signaling mechanisms. Mol. Cancer Ther., 2004, 3, 1671-1680.
122. Johnson, A.J.; Hsu, A.L.; Lin, H.P.; Song, X.; Chen, C.S. Thecyclo-oxygenase-2 inhibitor celecoxib perturbs intracellularcalcium by inhibiting endoplasmic reticulum Ca2+-ATPases: aplausible link with its anti-tumour effect and cardiovascular risks.Biochem. J., 2002, 366, 831-837.
123. Arico, S.; Pattingre, S.; Bauvy, C.; Gane, P.; Barbat, A.; Codogno, P.; Ogier-Denis, E. Celecoxib induces apoptosis by inhibiting 3-phosphoinositide-dependent protein kinase-1 activity in the humancolon cancer HT-29 cell line. J. Biol. Chem., 2002, 277, 27613-27621.
124. Lu, W.; Tinsley, H.N.; Keeton, A.; Qu, Z.; Piazza, G.A.; Li, Y.Suppression of Wnt/beta-catenin signaling inhibits prostate cancercell proliferation. Eur. J. Pharmacol., 2009, 602, 8-14.
125. Tuynman, J.B.; Vermeulen, L.; Boon, E.M.; Kemper, K.; Zwinderman, A.H.; Peppelenbosch, M.P.; Richel, D.J.Cyclooxygenase-2 inhibition inhibits c-Met kinase activity and Wnt activity in colon cancer. Cancer Res., 2008, 68, 1213-1220.
126. Abdulhameed, M.D.; Hamza, A.; Zhan, C.G. Microscopic modesand free energies of 3-phosphoinositide-dependent kinase-1(PDK1) binding with celecoxib and other inhibitors. J. Phys. Chem.B, 2006, 110, 26365-26374.
127. Minniti, G.; Muni, R.; Lanzetta, G.; Marchetti, P.; Enrici, R.M.Chemotherapy for glioblastoma: current treatment and futureperspectives for cytotoxic and targeted agents. Anticancer Res., 2009, 29, 5171-5184.
128. Pelloski, C.E.; Lin, E.; Zhang, L.; Yung, W.K.; Colman, H.; Liu, J.L.; Woo, S.Y.; Heimberger, A.B.; Suki, D.; Prados, M.; Chang, S.; Barker, F.G., 3rd; Fuller, G.N.; Aldape, K.D. Prognosticassociations of activated mitogen-activated protein kinase and Aktpathways in glioblastoma. Clin. Cancer Res., 2006, 12, 3935-3941.
129. Hambardzumyan, D.; Squatrito, M.; Carbajal, E.; Holland, E.C.Glioma formation, cancer stem cells, and akt signaling. Stem CellRev., 2008, 4, 203-210.
130. Hsu, A.L.; Ching, T.T.; Wang, D.S.; Song, X.; Rangnekar, V.M.; Chen, C.S. The cyclooxygenase-2 inhibitor celecoxib inducesapoptosis by blocking Akt activation in human prostate cancer cellsindependently of Bcl-2. J. Biol. Chem., 2000, 275, 11397-11403.
131. Leng, J.; Han, C.; Demetris, A.J.; Michalopoulos, G.K.; Wu, T.Cyclooxygenase-2 promotes hepatocellular carcinoma cell growththrough Akt activation: evidence for Akt inhibition in celecoxibinducedapoptosis. Hepatology, 2003, 38, 756-768.
132. Wu, T.; Leng, J.; Han, C.; Demetris, A.J. The cyclooxygenase-2inhibitor celecoxib blocks phosphorylation of Akt and inducesapoptosis in human cholangiocarcinoma cells. Mol. Cancer Ther., 2004, 3, 299-307.
133. Chen, Z.; Zhang, X.; Li, M.; Wang, Z.; Wieand, H.S.; Grandis, J.R.; Shin, D.M. Simultaneously targeting epidermal growth factorreceptor tyrosine kinase and cyclooxygenase-2, an efficientapproach to inhibition of squamous cell carcinoma of the head and neck. Clin. Cancer Res., 2004, 10, 5930-5939.
134. Hamdulay, S.S.; Wang, B.; Birdsey, G.M.; Ali, F.; Dumont, O.; Evans, P.C.; Haskard, D.O.; Wheeler-Jones, C.P.; Mason, J.C.Celecoxib activates PI-3K/Akt and mitochondrial redox signalingto enhance heme oxygenase-1-mediated anti-inflammatory activityin vascular endothelium. Free Radic. Biol. Med., 2010, 48, 1013-1023.
135. Peifer, C.; Alessi, D.R. Small-molecule inhibitors of PDK1. Chem.Med. Chem., 2008, 3, 1810-1838.
136. Williams, M.R.; Arthur, J.S.; Balendran, A.; van der Kaay, J.; Poli, V.; Cohen, P.; Alessi, D.R. The role of 3-phosphoinositidedependentprotein kinase 1 in activating AGC kinases defined inembryonic stem cells. Curr. Biol., 2000, 10, 439-448.
137. Ding, H.; Han, C.; Zhu, J.; Chen, C.S.; D'Ambrosio, S.M.Celecoxib derivatives induce apoptosis via the disruption of mitochondrial membrane potential and activation of caspase 9. Int.J. Cancer, 2005, 113, 803-810.
138. Knudsen, J.F.; Carlsson, U.; Hammarstrom, P.; Sokol, G.H.; Cantilena, L.R. The cyclooxygenase-2 inhibitor celecoxib is apotent inhibitor of human carbonic anhydrase II. Inflammation, 2004, 28, 285-290.
139. Weber, A.; Casini, A.; Heine, A.; Kuhn, D.; Supuran, C.T.; Scozzafava, A.; Klebe, G. Unexpected nanomolar inhibition of carbonic anhydrase by COX-2-selective celecoxib: newpharmacological opportunities due to related binding siterecognition. J. Med. Chem., 2004, 47, 550-557.
140. Di Fiore, A.; Pedone, C.; D'Ambrosio, K.; Scozzafava, A.; DeSimone, G.; Supuran, C.T. Carbonic anhydrase inhibitors: Valdecoxib binds to a different active site region of the humanisoform II as compared to the structurally related cyclooxygenase II"selective" inhibitor celecoxib. Bioorg. Med. Chem. Lett., 2006, 16, 437-442.
141. Supuran, C.T.; Scozzafava, A.; Casini, A. Carbonic anhydraseinhibitors. Med. Res. Rev., 2003, 23, 146-189.
142. Stocker, F.W. Use of carbonic anhydrase inhibitor acetazoleamide(diamox) for endothelial corneal dystrophy and diseased cornealgrafts. Trans. Am. Ophthalmol. Soc., 1955, 53, 175-180.
143. Pastorekova, S.; Kopacek, J.; Pastorek, J. Carbonic anhydraseinhibitors and the management of cancer. Curr. Top. Med. Chem., 2007, 7, 865-878.
144. Supuran, C.T. Carbonic anhydrases: novel therapeutic applicationsfor inhibitors and activators. Nat. Rev. Drug Discov., 2008, 7, 168-181.
145. Potter, C.P.; Harris, A.L. Diagnostic, prognostic and therapeuticimplications of carbonic anhydrases in cancer. Br. J. Cancer, 2003, 89, 2-7.
146. Jensen, R.L. Brain tumor hypoxia: tumorigenesis, angiogenesis, imaging, pseudoprogression, and as a therapeutic target. J.Neurooncol., 2009, 92, 317-335.
147. Ivanov, S.; Liao, S.Y.; Ivanova, A.; Danilkovitch-Miagkova, A.; Tarasova, N.; Weirich, G.; Merrill, M.J.; Proescholdt, M.A.; Oldfield, E.H.; Lee, J.; Zavada, J.; Waheed, A.; Sly, W.; Lerman, M.I.; Stanbridge, E.J. Expression of hypoxia-inducible cell-surfacetransmembrane carbonic anhydrases in human cancer. Am. J.Pathol., 2001, 158, 905-919.
148. Said, H.M.; Hagemann, C.; Staab, A.; Stojic, J.; Kuhnel, S.; Vince, G.H.; Flentje, M.; Roosen, K.; Vordermark, D. Expression patternsof the hypoxia-related genes osteopontin, CA9, erythropoietin, VEGF and HIF-1alpha in human glioma in vitro and in vivo.Radiother. Oncol., 2007, 83, 398-405.
149. Sathornsumetee, S.; Cao, Y.; Marcello, J.E.; Herndon, J.E., 2nd; McLendon, R.E.; Desjardins, A.; Friedman, H.S.; Dewhirst, M.W.; Vredenburgh, J.J.; Rich, J.N. Tumor angiogenic and hypoxicprofiles predict radiographic response and survival in malignantastrocytoma patients treated with bevacizumab and irinotecan. J.Clin. Oncol., 2008, 26, 271-278.
150. Reardon, D.A.; Desjardins, A.; Vredenburgh, J.J.; Gururangan, S.; Sampson, J.H.; Sathornsumetee, S.; McLendon, R.E.; Herndon, J.E., 2nd; Marcello, J.E.; Norfleet, J.; Friedman, A.H.; Bigner, D.D.; Friedman, H.S. Metronomic chemotherapy with daily, oraletoposide plus bevacizumab for recurrent malignant glioma: aphase II study. Br. J. Cancer, 2009, 101, 1986-1994.
151. Schönthal, A.H. Endoplasmic reticulum stress and autophagy astargets for cancer therapy. Cancer Lett., 2008, 275, 163-169.
152. Ma, Y.; Hendershot, L.M. The role of the unfolded proteinresponse in tumour development: friend or foe? Nat. Rev. Cancer, 2004, 4, 966-977.
153. Pyrko, P.; Schönthal, A.H.; Hofman, F.M.; Chen, T.C.; Lee, A.S.The unfolded protein response regulator GRP78/BiP as a noveltarget for increasing chemosensitivity in malignant gliomas.Cancer Res., 2007, 67, 9809-9816.
154. Boyce, M.; Yuan, J. Cellular response to endoplasmic reticulumstress: a matter of life or death. Cell Death Differ., 2006, 13, 363-373.
155. Lee, A.S. GRP78 induction in cancer: therapeutic and prognosticimplications. Cancer Res., 2007, 67, 3496-3499.
156. Oyadomari, S.; Mori, M. Roles of CHOP/GADD153 inendoplasmic reticulum stress. Cell Death Differ., 2004, 11, 381-389.
157. Tsutsumi, S.; Gotoh, T.; Tomisato, W.; Mima, S.; Hoshino, T.; Hwang, H.J.; Takenaka, H.; Tsuchiya, T.; Mori, M.; Mizushima, T.Endoplasmic reticulum stress response is involved in nonsteroidalanti-inflammatory drug-induced apoptosis. Cell Death Differ., 2004, 11, 1009-1016.
158. Tsutsumi, S.; Namba, T.; Tanaka, K.I.; Arai, Y.; Ishihara, T.; Aburaya, M.; Mima, S.; Hoshino, T.; Mizushima, T. Celecoxibupregulates endoplasmic reticulum chaperones that inhibitcelecoxib-induced apoptosis in human gastric cells. Oncogene, 2006, 25, 1018-1029.
159. Kim, S.H.; Hwang, C.I.; Park, W.Y.; Lee, J.H.; Song, Y.S.GADD153 mediates celecoxib-induced apoptosis in cervical cancercells. Carcinogenesis, 2007, 28, 223-231.
160. Chen, S.T.; Thomas, S.; Gaffney, K.J.; Louie, S.G.; Petasis, N.A.; Schonthal, A.H. Cytotoxic effects of celecoxib on Raji lymphomacells correlate with aggravated endoplasmic reticulum stress but notwith inhibition of cyclooxygenase-2. Leuk. Res., 2010, 34, 250-253.
161. Pyrko, P.; Kardosh, A.; Schönthal, A.H. Celecoxib transientlyinhibits protein synthesis. Biochem. Pharmacol., 2008, 75, 395-404.
162. Pyrko, P.; Kardosh, A.; Wang, W.; Xiong, W.; Schönthal, A.H.; Chen, T.C. HIV protease inhibitors nelfinavir and atazanavirinduce glioblastoma cell death by triggering endoplasmic reticulum(ER) stress. Cancer Res., 2007, 67, 10920-10928.
163. Lee, A.S.; Hendershot, L.M. ER stress and cancer. Cancer Biol.Ther., 2006, 5, 721-722.
164. Hiss, D.C.; Gabriels, G.A. Implications of endoplasmic reticulumstress, the unfolded protein response and apoptosis for molecularcancer therapy. Expert Opin. Drug Discov., 2009, 4, 799-821.
165. Alloza, I.; Baxter, A.; Chen, Q.; Matthiesen, R.; Vandenbroeck, K.Celecoxib inhibits interleukin-12 alphabeta and beta2 folding and secretion by a novel COX2-independent mechanism involvingchaperones of the endoplasmic reticulum. Mol. Pharmacol., 2006, 69, 1579-1587.
166. Tanaka, K.; Tomisato, W.; Hoshino, T.; Ishihara, T.; Namba, T.; Aburaya, M.; Katsu, T.; Suzuki, K.; Tsutsumi, S.; Mizushima, T.Involvement of intracellular Ca2+ levels in nonsteroidal antiinflammatorydrug-induced apoptosis. J. Biol. Chem., 2005, 280, 31059-31067.
167. Wang, J.L.; Lin, K.L.; Chen, J.S.; Lu, Y.C.; Jiann, B.P.; Chang, H.T.; Hsu, S.S.; Chen, W.C.; Huang, J.K.; Ho, C.M.; Jan, C.R.Effect of celecoxib on Ca2+ movement and cell proliferation inhuman osteoblasts. Biochem. Pharmacol., 2004, 67, 1123-1130.
168. Denmeade, S.R.; Isaacs, J.T. The SERCA pump as a therapeutictarget: making a "smart bomb" for prostate cancer. Cancer Biol.Ther., 2005, 4, 14-22.
169. Deng, J.; Lu, P.D.; Zhang, Y.; Scheuner, D.; Kaufman, R.J.; Sonenberg, N.; Harding, H.P.; Ron, D. Translational repressionmediates activation of nuclear factor kappa B by phosphorylatedtranslation initiation factor 2. Mol. Cell Biol., 2004, 24, 10161-10168.
170. Kern, M.A.; Haugg, A.M.; Koch, A.F.; Schilling, T.; Breuhahn, K.; Walczak, H.; Fleischer, B.; Trautwein, C.; Michalski, C.; Schulze-Bergkamen, H.; Friess, H.; Stremmel, W.; Krammer, P.H.; Schirmacher, P.; Müller, M. Cyclooxygenase-2 inhibition inducesapoptosis signaling via death receptors and mitochondria inhepatocellular carcinoma. Cancer Res., 2006, 66, 7059-7066.
171. Chen, S.; Liu, X.; Yue, P.; Schonthal, A.H.; Khuri, F.R.; Sun, S.Y.CCAAT/enhancer binding protein homologous protein-dependentdeath receptor 5 induction and ubiquitin/proteasome-mediatedcellular FLICE-inhibitory protein down-regulation contribute toenhancement of tumor necrosis factor-related apoptosis-inducingligand-induced apoptosis by dimethyl-celecoxib in human nonsmall-cell lung cancer cells. Mol. Pharmacol., 2007, 72, 1269-1279.
172. Liu, X.; Yue, P.; Schonthal, A.H.; Khuri, F.R.; Sun, S.Y. CellularFLICE-inhibitory protein down-regulation contributes to celecoxibinducedapoptosis in human lung cancer cells. Cancer Res., 2006, 66, 11115-11119.
173. Yamaguchi, H.; Wang, H.G. CHOP is involved in endoplasmicreticulum stress-induced apoptosis by enhancing DR5 expression inhuman carcinoma cells. J. Biol. Chem., 2004, 279, 45495-45502.
174. He, Q.; Lee, D.I.; Rong, R.; Yu, M.; Luo, X.; Klein, M.; El-Deiry, W.S.; Huang, Y.; Hussain, A.; Sheikh, M.S. Endoplasmicreticulum calcium pool depletion-induced apoptosis is coupled withactivation of the death receptor 5 pathway. Oncogene, 2002, 21, 2623-2633.
175. Davies, N.M.; McLachlan, A.J.; Day, R.O.; Williams, K.M.Clinical pharmacokinetics and pharmacodynamics of celecoxib: aselective cyclo-oxygenase-2 inhibitor. Clin. Pharmacokinet., 2000, 38, 225-242.
176. Raz, A. Is inhibition of cyclooxygenase required for the antitumorigeniceffects of nonsteroidal, anti-inflammatory drugs(NSAIDs)? In vitro versus in vivo results and the relevance for theprevention and treatment of cancer. Biochem. Pharmacol., 2002, 63, 343-347.
177. Maier, T.J.; Schiffmann, S.; Wobst, I.; Birod, K.; Angioni, C.; Hoffmann, M.; Lopez, J.J.; Glaubitz, C.; Steinhilber, D.; Geisslinger, G.; Grosch, S. Cellular membranes function as astorage compartment for celecoxib. J. Mol. Med., 2009, 87, 981-993.
178. Clinical Trials.gov - A Service of the U.S. National Institutes of Health. http://www.clinicaltrials.gov/ (Accessed August 2, 2010).