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Preventive but Not Curative Efficacy of Celecoxib on Bladder Carcinogenesis in a Rat Model

DOI: 10.1155/2010/380937

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Abstract:

To evaluate the effect of a cyclooxygenase 2 inhibitor, celecoxib (CEL), on bladder cancer inhibition in a rat model, when used as preventive versus as curative treatment. The study comprised 52 male Wistar rats, divided in 5 groups, during a 20-week protocol: control: vehicle, carcinogen: 0.05% of N-butyl-N-(4-hydroxybutyl) nitrosamine (BBN), CEL: 10？mg/kg/day of the selective COX-2 inhibitor Celebrex, preventive CEL (CEL+BBN-P), and curative CEL (BBN+CEL-C) groups. Although tumor growth was markedly inhibited by the preventive application of CEL, it was even aggravated by the curative treatment. The incidence of gross bladder carcinoma was: control 0/8(0%), BBN 13/20(65%), CEL 0/8(0%), CEL+BBN-P 1/8(12.5%), and BBN+CEL-C 6/8(75%). The number and volume of carcinomas were significantly lower in the CEL+BBN-P versus BBN, accompanied by an ample reduction in hyperplasia, dysplasia, and papillary tumors as well as COX-2 immunostaining. In spite of the reduction of tumor volumes in the curative BBN+CEL-C group, tumor malignancy was augmented. An anti-inflammatory and antioxidant profile was encountered only in the group under preventive treatment. In conclusion, preventive, but not curative, celecoxib treatment promoted a striking inhibitory effect on bladder cancer development, reinforcing the potential role of chemopreventive strategies based on cyclooxygenase 2 inhibition. 1. Introduction Bladder cancer is a prevalent tumor, accounting for 5%–10% of all malignancies in Western countries [1, 2]. It has a high recurrence and progression rate and the prognosis, except for superficial forms, is poor [3]. Furthermore, it has high mortality rates and socioeconomic costs [4, 5]. The conventional surgical techniques and therapeutic options might cause discomfort to patients, especially in invasive and aggressive forms of cancer [6, 7]. Therefore, the improvement of bladder cancer management and treatment could rely on better preventive strategies. The identification of promising drugs remains dependent on a better elucidation of the molecular/cellular mechanisms underlying cancer appearance and progression [8, 9]. Apart from the genetic features and markers already characterized [10, 11], the cellular and molecular mechanisms for development and/or progression might involve inflammatory, proliferative, and oxidative stress phenomena that should be better elucidated. Inflammation through the cyclooxygenase (COX) pathway has been involved in cancer development [12]. While COX-1 is constitutively expressed in a huge range of tissues, playing a role in

 References

[1]  Z. Kirkali, T. Chan, M. Manoharan et al., “Bladder cancer: epidemiology, staging and grading, and diagnosis,” Urology, vol. 66, no. 6, supplement, pp. 4–34, 2005.
[2]  J. Ferlay, P. Autier, M. Boniol, M. Heanue, M. Colombet, and P. Boyle, “Estimates of the cancer incidence and mortality in Europe in 2006,” Annals of Oncology, vol. 18, no. 3, pp. 581–592, 2007.
[3]  K. Matsumoto, A. Irie, T. Satoh, H. Kuruma, T. Arakawa, and S. Baba, “Occupational bladder cancer: from cohort study to biologic molecular marker,” Medical Science Monitor, vol. 11, no. 10, pp. RA311–RA315, 2005.
[4]  V. K. Sangar, N. Ragavan, S. S. Matanhelia, M. W. Watson, and R. A. Blades, “The economic consequences of prostate and bladder cancer in the UK,” BJU International, vol. 95, no. 1, pp. 59–63, 2005.
[5]  M. Grasso, “Bladder cancer: a major public health issue,” European Urology, Supplements, vol. 7, no. 7, pp. 510–515, 2008.
[6]  R. J. Sylvester, A. P. M. Van Der Meijden, W. Oosterlinck et al., “Predicting recurrence and progression in individual patients with stage Ta T1 bladder cancer using EORTC risk tables: a combined analysis of 2596 patients from seven EORTC trials,” European Urology, vol. 49, no. 3, pp. 466–475, 2006.
[7]  S. B. Malkowicz, H. van Poppel, G. Mickisch et al., “Muscle-invasive urothelial carcinoma of the bladder,” Urology, vol. 69, no. 1, supplement, pp. 3–16, 2007.
[8]  S. F. Shariat, J. H. Kim, G. E. Ayala, K. Kho, T. M. Wheeler, and S. P. Lerner, “Cyclooxygenase-2 is highly expressed in carcinoma in situ and T1 transitional cell carcinoma of the bladder,” Journal of Urology, vol. 169, no. 3, pp. 938–942, 2003.
[9]  R. Baffa, J. Letko, C. McClung, J. LeNoir, A. Vecchione, and L. G. Gomella, “Molecular genetics of bladder cancer: targets for diagnosis and therapy,” Journal of Experimental and Clinical Cancer Research, vol. 25, no. 2, pp. 145–160, 2006.
[10]  D. J. Wolff, “The genetics of bladder cancer: a cytogeneticist's perspective,” Cytogenetic and Genome Research, vol. 118, no. 2–4, pp. 177–181, 2007.
[11]  D. Ahirwar, A. Mandhani, and R. D. Mittal, “Interleukin-10 G-1082A and C-819T polymorphisms as possible molecular markers of urothelial bladder cancer,” Archives of Medical Research, vol. 40, no. 2, pp. 97–102, 2009.
[12]  R. E. Harris, “Cyclooxygenase-2 (cox-2) and the inflammogenesis of cancer,” Sub-Cellular Biochemistry, vol. 42, pp. 93–126, 2007.
[13]  P. C. A. Kam and A. U. L. See, “Cyclo-oxygenase isoenzymes: physiological and pharmacological role,” Anaesthesia, vol. 55, no. 5, pp. 442–449, 2000.
[14]  J. M. Di, J. Zhou, X. L. Zhou et al., “Cyclooxygenase-2 expression is associated with vascular endothelial growth factor-C and lymph node metastases in human prostate cancer,” Archives of Medical Research, vol. 40, no. 4, pp. 268–275, 2009.
[15]  A. Sengupta, S. Ghosh, R. K. Das, S. Bhattacharjee, and S. Bhattacharya, “Chemopreventive potential of diallylsulfide, lycopene and theaflavin during chemically induced colon carcinogenesis in rat colon through modulation of cyclooxygenase-2 and inducible nitric oxide synthase pathways,” European Journal of Cancer Prevention, vol. 15, no. 4, pp. 301–305, 2006.
[16]  L. S. Fournier, V. Novikov, V. Lucidi et al., “MR monitoring of cyclooxygenase-2 inhibition of angiogenesis in a human breast cancer model in rats,” Radiology, vol. 243, no. 1, pp. 105–111, 2007.
[17]  R. W. Stockbrügger, “Nonsteroidal anti-inflammatory drugs (NSAIDs) in the prevention of colorectal cancer,” European Journal of Cancer Prevention, vol. 8, no. 1, supplement, pp. S21–S25, 1999.
[18]  W. Kitayama, A. Denda, E. Okajima, T. Tsujiuchi, and Y. Konishi, “Increased expression of cyclooxygenase-2 protein in rat urinary bladder tumors induced by N-butyl-N-(4-hydroxybutyl) nitrosamine,” Carcinogenesis, vol. 20, no. 12, pp. 2305–2310, 1999.
[19]  T. Shirahama, “Cyclooxygenase-2 expression is up-regulated in transitional cell carcinoma and its preneoplastic lesions in the human urinary bladder,” Clinical Cancer Research, vol. 6, no. 6, pp. 2424–2430, 2000.
[20]  A. Ristim？ki, O. Nieminen, K. Saukkonen, K. Hotakainen, S. Nordling, and C. Haglund, “Expression of cyclooxygenase-2 in human transitional cell carcinoma of the urinary bladder,” American Journal of Pathology, vol. 158, no. 3, pp. 849–853, 2001.
[21]  R. D. Klein, C. S. Van Pelt, A. L. Sabichi et al., “Transitional cell hyperplasia and carcinomas in urinary bladders of transgenic mice with keratin 5 promoter-driven cyclooxygenase-2 overexpression,” Cancer Research, vol. 65, no. 5, pp. 1808–1813, 2005.
[22]  B. Parada, J. Sereno, F. Reis et al., “Anti-inflammatory, anti-proliferative and antioxidant profiles of selective cyclooxygenase-2 inhibition as chemoprevention for rat bladder carcinogenesis,” Cancer Biology and Therapy, vol. 8, no. 17, pp. 1615–1622, 2009.
[23]  S. Fukushima, M. Hirose, and H. Tsuda, “Histological classification of urinary bladder cancers in rats induced by N butyl N (4 hydroxybutyl)nitrosamine,” Gann, The Japanese Journal of Cancer Research, vol. 67, no. 1, pp. 81–90, 1976.
[24]  R. Montironi and R. Mazzucchelli, “Preneoplastic lesions and conditions of the urinary bladder,” EAU Update Series, vol. 1, no. 2, pp. 53–63, 2003.
[25]  G. Sauter, F. Algaba, and M. Amin, “Tumors of the urinary system: non-invasive urothelial neoplasias,” in WHO Classification of Tumors of the Urinary System and Male Genital Organs, J. N. Eble, G. Sauter, J. L. Epstein, and I. Sesterhenn, Eds., pp. 29–34, IARCC Press, Lyon, France, 2004.
[26]  J. T. Leppert, O. Shvarts, K. Kawaoka, R. Lieberman, A. S. Belldegrun, and A. J. Pantuck, “Prevention of bladder cancer: a review,” European Urology, vol. 49, no. 2, pp. 226–234, 2006.
[27]  V. Estepa, S. Ródenas, and M. C. Martín, “Optimización de un método para la determinación de la peroxidación lipidica en suero humano,” Anales de la Real Academia de Farmacia, vol. 67, no. 3, pp. 1–17, 2001.
[28]  I. F. F. Benzie and J. J. Strain, “The ferric reducing ability of plasma (FRAP) as a measure of “antioxidant power“: the FRAP assay,” Analytical Biochemistry, vol. 239, no. 1, pp. 70–76, 1996.
[29]  C. J. Grubbs, R. A. Lubet, A. T. Koki et al., “Celecoxib inhibits N-butyl-N-(4-hydroxybutyl)-nitrosamine-induced urinary bladder cancers in male B6D2F1 mice and female Fischer-344 rats,” Cancer Research, vol. 60, no. 20, pp. 5599–5602, 2000.
[30]  H. Süleyman, B. Demircan, and Y. Karag？z, “Anti-inflammatory and side effects of cyclooxygenase inhibitors,” Pharmacological Reports, vol. 59, no. 3, pp. 247–258, 2007.
[31]  A. L. Hsu, T. T. Ching, D. S. Wang, X. Song, V. M. Rangnekar, and C. S. Chen, “The cyclooxygenase-2 inhibitor celecoxib induces apoptosis by blocking Akt activation in human prostate cancer cells independently of Bcl-2,” The Journal of Biological Chemistry, vol. 275, no. 15, pp. 11397–11403, 2000.
[32]  X. Song, H. P. Lin, A. J. Johnson et al., “Cyclooxygenase-2, player or spectator in cyclooxygenase-2 inhibitor-induced apoptosis in prostate cancer cells,” Journal of the National Cancer Institute, vol. 94, no. 8, pp. 585–591, 2002.
[33]  X. H. Liu, A. Kirschenbaum, S. Yao, R. Lee, J. F. Holland, and A. C. Levine, “Inhibition of cyclooxygenase-2 suppresses angiogenesis and the growth of prostate cancer in vivo,” Journal of Urology, vol. 164, no. 3, pp. 820–825, 2000.
[34]  B. A. Narayanan, M. S. Condon, M. C. Bosland, N. K. Narayanan, and B. S. Reddy, “Suppression of N-methyl-N-nitrosourea/testosterone-induced rat prostate cancer growth by celecoxib: effects on cyclooxygenase-2, cell cycle regulation, and apoptosis mechanism(s),” Clinical Cancer Research, vol. 9, no. 9, pp. 3503–3513, 2003.
[35]  V. Vital-Reyes, C. Rodríguez-Burford, D. C. Chhieng et al., “Celecoxib inhibits cellular growth, decreases Ki-67 expression and modifies apoptosis in ovarian cancer cell lines,” Archives of Medical Research, vol. 37, no. 6, pp. 689–695, 2006.
[36]  A. Federico, F. Morgillo, C. Tuccillo, F. Ciardiello, and C. Loguercio, “Chronic inflammation and oxidative stress in human carcinogenesis,” International Journal of Cancer, vol. 121, no. 11, pp. 2381–2386, 2007.
[37]  A. M. Lewis, S. Varghese, H. Xu, and H. R. Alexander, “Interleukin-1 and cancer progression: the emerging role of interleukin-1 receptor antagonist as a novel therapeutic agent in cancer treatment,” Journal of Translational Medicine, vol. 4, article 48, 2006.
[38]  C. A. Dinarello, “Why not treat human cancer with interleukin-1 blockade?” Cancer and Metastasis Reviews, vol. 29, no. 2, pp. 317–329, 2010.
[39]  B. S. Reddy, Y. Hirose, R. Lubet et al., “Chemoprevention of colon cancer by specific cyclooxygenase-2 inhibitor, celecoxib, administered during different stages of carcinogenesis,” Cancer Research, vol. 60, no. 2, pp. 293–297, 2000.

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