Nonsteroidal anti-inflammatory drugs and prostatic diseases

Hitoshi Ishiguro, Takashi Kawahara, Hitoshi Ishiguro, Takashi Kawahara

Abstract

Prostatic diseases are characterized by increased activity of cytokines, growth factors, and cyclooxygenases- (COX-) 1 and 2. Activation of COX-1 and COX-2 results in increased levels of prostaglandins and the induction of angiogenic, antiapoptotic and inflammatory processes. Inhibition of COX enzymes by members of the widely used nonsteroidal anti-inflammatory drug (NSAID) class of drugs decreases prostaglandin production, and exerts a variety of anti-inflammatory, antipyretic, and antinociceptive effects. While numerous in vitro, in vivo, and clinical studies have shown that NSAIDs inhibit the risk and progression of prostatic diseases, the relationship between NSAIDs and such diseases remains controversial. Here we review the literature in this area, critically analyzing the benefits and caveats associated with the use of NSAIDs in the treatment of prostatic diseases.

Figures

Figure 1
Figure 1
Schematic of the mechanism of action of NSAIDs. NSAID inhibition of cyclooxygenase-1 and/or cyclooxygenase-2 suppresses prostaglandin G2 production, promoting apoptosis and blocking angiogenesis, inflammation, and tumor progression.

References

    1. Schrecengost R, Knudsen KE. Molecular pathogenesis and progression of prostate cancer. Seminars in Oncology. 2013;40(3):244–258.
    1. Penna G, Mondaini N, Amuchastegui S, et al. Seminal plasma cytokines and chemokines in prostate inflammation: interleukin 8 as a predictive biomarker in chronic prostatitis/chronic pelvic pain syndrome and benign prostatic hyperplasia. European Urology. 2007;51(2):524–533.
    1. Macoska JA. Chemokines and BPH/LUTS. Differentiation. 2011;82(4-5):253–260.
    1. Cai T, Mazzoli S, Meacci F, et al. Epidemiological features and resistance pattern in uropathogens isolated from chronic bacterial prostatitis. The Journal of Microbiology. 2011;49(3):448–454.
    1. Vane JR. Inhibition of prostaglandin synthesis as a mechanism of action for aspirin-like drugs. Nature. 1971;231(25):232–235.
    1. DuBois RN, Abramson SB, Crofford L, et al. Cyclooxygenase in biology and disease. The FASEB Journal. 1998;12(12):1063–1073.
    1. Vane JR, Bakhle YS, Botting RM. Cyclooxygenases 1 and 2. Annual Review of Pharmacology and Toxicology. 1998;38:97–120.
    1. Bombardier C, Laine L, Reicin A, et al. Comparison of upper gastrointestinal toxicity of rofecoxib and naproxen in patients with rheumatoid arthritis. The New England Journal of Medicine. 2000;343(21):1520–1528.
    1. Bresalier RS, Sandler RS, Quan H, et al. Cardiovascular events associated with rofecoxib in a colorectal adenoma chemoprevention trial. The New England Journal of Medicine. 2005;352(11):1092–1102.
    1. Rigas B, Kashfi K. Nitric-oxide-donating NSAIDs as agents for cancer prevention. Trends in Molecular Medicine. 2004;10(7):324–330.
    1. Krieger JN, Nyberg L, Jr., Nickel JC. NIH consensus definition and classification of prostatitis. The Journal of the American Medical Association. 1999;282(3):236–237.
    1. Canale D, Scaricabarozzi I, Giorgi P, Turchi P, Ducci M, Menchini-Fabris GF. Use of a novel non-steroidal anti-inflammatory drug, nimesulide, in the treatment of abacterial prostatovesiculitis. Andrologia. 1993;25(3):163–166.
    1. Nickel JC, Pontari M, Moon T, et al. A randomized, placebo controlled, multicenter study to evaluate the safety and efficacy of rofecoxib in the treatment of chronic nonbacterial prostatitis. The Journal of Urology. 2003;169(4):1401–1405.
    1. Parsons JK. Benign prostatic hyperplasia and male lower urinary tract symptoms: epidemiology and risk factors. Current Bladder Dysfunction Reports. 2010;5(4):212–218.
    1. Nickel JC. Inflammation and benign prostatic hyperplasia. Urologic Clinics of North America. 2008;35(1):109–115.
    1. Chughtai B, Lee R, Te A, Kaplan S. Role of inflammation in benign prostatic hyperplasia. Reviews in Urology. 2011;13(3):147–150.
    1. Kohnen PW, Drach GW. Patterns of inflammation in prostatic hyperplasia: a histologic and bacteriologic study. The Journal of Urology. 1979;121(6):755–760.
    1. di Silverio F, Gentile V, de Matteis A, et al. Distribution of inflammation, pre-malignant lesions, incidental carcinoma in histologically confirmed benign prostatic hyperplasia: a retrospective analysis. European Urology. 2003;43(2):164–175.
    1. Steiner GE, Newman ME, Paikl D, et al. Expression and function of pro-inflammatory interleukin IL-17 and IL-17 receptor in normal, benign hyperplastic, and malignant prostate. The Prostate. 2003;56(3):171–182.
    1. O'Neill GP, Ford-Hutchinson AW. Expression of mRNA for cyclooxygenase-1 and cyclooxygenase-2 in human tissues. FEBS Letters. 1993;330(2):156–160.
    1. Kirschenbaum A, Klausner AP, Lee R, et al. Expression of cyclooxygenase-1 and cyclooxygenase-2 in the human prostate. Urology. 2000;56(4):671–676.
    1. Lee L-M, Pan C-C, Cheng C-J, Chi C-W, Liu T-Y. Expression of cyclooxygenase-2 in prostate adenocarcinoma and benign prostatic hyperplasia. Anticancer Research. 2001;21(2):1291–1294.
    1. Wang W, Bergh A, Damber J-E. Chronic inflammation in benign prostate hyperplasia is associated with focal upregulation of cyclooxygenase-2, Bcl-2, and cell proliferation in the glandular epithelium. The Prostate. 2004;61(1):60–72.
    1. di Silverio F, Bosman C, Salvatori M, et al. Combination therapy with rofecoxib and finasteride in the treatment of men with Lower Urinary Tract Symptoms (LUTS) and Benign Prostatic Hyperplasia (BPH) European Urology. 2005;47(1):72–79.
    1. Ozdemir I, Bozkurt O, Demir O, Aslan G, Esen AA. Combination therapy with doxazosin and tenoxicam for the management of lower urinary tract symptoms. Urology. 2009;74(2):431–435.
    1. Jhang J-F, Jiang Y-H, Kuo H-C. Adding cyclooxygenase-2 inhibitor to alpha blocker for patients with benign prostate hyperplasia and elevated serum prostate specific antigen could not improve prostate biopsy detection rate but improve lower urinary tract symptoms. International Journal of Clinical Practice. 2013;67(12):1327–1333.
    1. Kaye M. Aging, circadian weight change, and nocturia. Nephron Physiology. 2008;109(1):p11–p18.
    1. St. Sauver JL, Jacobson DJ, Mcgree ME, Lieber MM, Jacobsen SJ. Protective association between nonsteroidal antiinflammatory drug use and measures of benign prostatic hyperplasia. American Journal of Epidemiology. 2006;164(8):760–768.
    1. Falahatkar S, Mokhtari G, Pourreza F, Asgari SA, Kamran AN. Celecoxib for treatment of nocturia caused by benign prostatic hyperplasia: a prospective, randomized, double-blind, placebo-controlled study. Urology. 2008;72(4):813–816.
    1. Kahokehr A, Vather R, Nixon A, Hill AG. Non-steroidal anti-inflammatory drugs for lower urinary tract symptoms in benign prostatic hyperplasia: systematic review and meta-analysis of randomized controlled trials. BJU International. 2013;111(2):304–311.
    1. Schenk JM, Calip GS, Tangen CM, et al. Indications for and use of nonsteroidal antiinflammatory drugs and the risk of incident, symptomatic benign prostatic hyperplasia: results from the prostate cancer prevention trial. American Journal of Epidemiology. 2012;176(2):156–163.
    1. Meigs JB, Mohr B, Barry MJ, Collins MM, McKinlay JB. Risk factors for clinical benign prostatic hyperplasia in a community-based population of healthy aging men. Journal of Clinical Epidemiology. 2001;54(9):935–944.
    1. Kang D, Andriole GL, van de Vooren RC, et al. Risk behaviours and benign prostatic hyperplasia. BJU International. 2004;93(9):1241–1245.
    1. Verhamme KMC, Dieleman JP, van Wijk MAM, et al. Nonsteroidal anti-inflammatory drugs and increased risk of acute urinary retention. Archives of Internal Medicine. 2005;165(13):1547–1551.
    1. Minnery CH, Getzenberg RH. Benign prostatic hyperplasia cell line viability and modulation of JM-27 by doxazosin and ibuprofen. The Journal of Urology. 2005;174(1):375–379.
    1. Altavilla D, Minutoli L, Polito F, et al. Effects of flavocoxid, a dual inhibitor of COX and 5-lipoxygenase enzymes, on benign prostatic hyperplasia. British Journal of Pharmacology. 2012;167(1):95–108.
    1. Kashiwagi E, Shiota M, Yokomizo A, et al. Prostaglandin receptor EP3 mediates growth inhibitory effect of aspirin through androgen receptor and contributes to castration resistance in prostate cancer cells. Endocrine-Related Cancer. 2013;20(3):431–441.
    1. de Marzo AM, Platz EA, Sutcliffe S, et al. Inflammation in prostate carcinogenesis. Nature Reviews Cancer. 2007;7(4):256–269.
    1. Sfanos KS, de Marzo AM. Prostate cancer and inflammation: the evidence. Histopathology. 2012;60(1):199–215.
    1. Haverkamp J, Charbonneau B, Ratliff TL. Prostate inflammation and its potential impact on prostate cancer: a current review. Journal of Cellular Biochemistry. 2008;103(5):1344–1353.
    1. Gupta S, Srivastava M, Ahmad N, Bostwick DG, Mukhtar H. Over-expression of cyclooxygenase-2 in human prostate adenocarcinoma. The Prostate. 2000;42(1):73–78.
    1. Majima M, Amano H, Hayashi I. Prostanoid receptor signaling relevant to tumor growth and angiogenesis. Trends in Pharmacological Sciences. 2003;24(10):524–529.
    1. Veitonmäki T, Tammela TL, Auvinen A, Murtola TJ. Use of aspirin, but not other non-steroidal anti-inflammatory drugs is associated with decreased prostate cancer risk at the population level. European Journal of Cancer. 2013;49(4):938–945.
    1. Patel MI, Subbaramaiah K, Du B, et al. Celecoxib inhibits prostate cancer growth: evidence of a cyclooxygenase-2-independent mechanism. Clinical Cancer Research. 2005;11(5):1999–2007.
    1. Hsu A-L, Ching T-T, Wang D-S, Song X, Rangnekar VM, Chen C-S. 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. 2000;275(15):11397–11403.
    1. Kulp SK, Yang Y-T, Hung C-C, et al. 3-phosphoinositide-dependent protein kinase-1/Akt signaling represents a major cyclooxygenase-2-independent target for celecoxib in prostate cancer cells. Cancer Research. 2004;64(4):1444–1451.
    1. Inoue T, Anai S, Onishi S, et al. Inhibition of COX-2 expression by topical diclofenac enhanced radiation sensitivity via enhancement of TRAIL in human prostate adenocarcinoma xenograft model. BMC Urology. 2013;13, article 1
    1. Zheng X, Cui X-X, Gao Z, et al. Atorvastatin and celecoxib in combination inhibits the progression of androgen-dependent LNCaP xenograft prostate tumors to androgen independence. Cancer Prevention Research. 2010;3(1):114–124.
    1. Abedinpour P, Baron VT, Welsh J, Borgström P. Regression of prostatetumors upon combination of hormone ablation therapy and celecoxib in vivo. The Prostate. 2011;71(8):813–823.
    1. Narayanan BA, Narayanan NK, Pittman B, Reddy BS. Regression of mouse prostatic intraepithelial neoplasia by nonsteroidal anti-inflammatory drugs in the transgenic adenocarcinoma mouse prostate model. Clinical Cancer Research. 2004;10(22):7727–7737.
    1. Gupta S, Adhami VM, Subbarayan M, et al. Suppression of prostate carcinogenesis by dietary supplementation of celecoxib in transgenic adenocarcinoma of the mouse prostate model. Cancer Research. 2004;64(9):3334–3343.
    1. Narayanan BA, Narayanan NK, Pttman B, Reddy BS. Adenocarcina of the mouse prostate growth inhibition by celecoxib: downregulation of transcription factors involved in COX-2 inhibition. The Prostate. 2006;66(3):257–265.
    1. Narayanan BA, Condon MS, Bosland MC, Narayanan NK, Reddy BS. 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. 2003;9(9):3503–3513.
    1. Royle JS, Ross JA, Ansell I, Bollina P, Tulloch DN, Habib FK. Nitric oxide donating nonsteroidal anti-inflammatory drugs induce apoptosis in human prostate cancer cell systems and human prostatic stroma via caspase-3. The Journal of Urology. 2004;172(1):338–344.
    1. Huguenin S, Fleury-Feith J, Kheuang L, et al. Nitrosulindac (NCX 1102): a new nitric oxide-donating non-steroidal anti-inflammatory drug (NO-NSAID), inhibits proliferation and induces apoptosis in human prostatic epithelial cell lines. The Prostate. 2004;61(2):132–141.
    1. Stewart GD, Nanda J, Brown DJG, Riddick ACP, Ross JA, Habib FK. NO-sulindac inhibits the hypoxia response of PC-3 prostate cancer cells via the Akt signalling pathway. International Journal of Cancer. 2009;124(1):223–232.
    1. Lu W, Tinsley HN, Keeton A, Qu Z, Piazza GA, Li Y. Suppression of Wnt/β-catenin signaling inhibits prostate cancer cell proliferation. European Journal of Pharmacology. 2009;602(1):8–14.
    1. Semenza GL. Targeting HIF-1 for cancer therapy. Nature Reviews Cancer. 2003;3(10):721–732.
    1. Nelson JE, Harris RE. Inverse association of prostate cancer and non-steroidal anti-inflammatory drugs (NSAIDs): results of a case-control study. Oncology Reports. 2000;7(1):169–170.
    1. Habel LA, Zhao W, Stanford JL. Daily aspirin use and prostate cancer risk in a large, multiracial cohort in the US. Cancer Causes & Control. 2002;13(5):427–434.
    1. Smith MR, Manola J, Kaufman DS, Oh WK, Bubley GJ, Kantoff PW. Celecoxib versus placebo for men with prostate cancer and a rising serum prostate-specific antigen after radical prostatectomy and/or radiation therapy. Journal of Clinical Oncology. 2006;24(18):2723–2728.
    1. Norrish AE, Jackson RT, McRae CU. Non-steroidal anti-inflammatory drugs and prostate cancer progression. International Journal of Cancer. 1998;77(4):511–515.
    1. Salinas CA, Kwon EM, Fitzgerald LM, et al. Use of aspirin and other nonsteroidal antiinflammatory medications in relation to prostate cancer risk. American Journal of Epidemiology. 2010;172(5):578–590.
    1. Roberts RO, Jacobson DJ, Girman CJ, Rhodes T, Lieber MM, Jacobsen SJ. A population-based study of daily nonsteroidal anti-inflammatory drug use and prostate cancer. Mayo Clinic Proceedings. 2002;77(3):219–225.
    1. Pruthi RS, Derksen JE, Moore D. A pilot study of use of the cyclooxygenase-2 inhibitor celecoxib in recurrent prostate cancer after definitive radiation therapy or radical prostatectomy. BJU International. 2004;93(3):275–278.
    1. Menezes RJ, Swede H, Niles R, Moysich KB. Regular use of aspirin and prostate cancer risk (United States) Cancer Causes & Control. 2006;17(3):251–256.
    1. Bosetti C, Talamini R, Negri E, Franceschi S, Montella M, la Vecchia C. Aspirin and the risk of prostate cancer. European Journal of Cancer Prevention. 2006;15(1):43–45.
    1. Langman MJS, Cheng KK, Gilman EA, Lancashire RJ. Effect of anti-inflammatory drugs on overall risk of common cancer: case-control study in general practice research database. British Medical Journal. 2000;320(7250):1642–1646.
    1. Leitzmann MF, Stampfer MJ, Ma J, et al. Aspirin use in relation to risk of prostate cancer. Cancer Epidemiology Biomarkers & Prevention. 2002;11(10):1108–1111.

Source: PubMed

Sponsor e collaboratori

Condizioni mediche

Interventi farmacologici

3
Sottoscrivi