#PAGE_PARAMS# #ADS_HEAD_SCRIPTS# #MICRODATA#

Acetylsalicylic Acid and its Potential for Chemoprevention of Colorectal Carcinoma


Authors: Podhorec Ján 1,2;  Hrstka Roman 1;  Bílek Ondřej 2;  Tuček Štěpán 2;  Navrátil Jiří 2;  Michalová Eva 1;  Vojtěšek Bořivoj 1
Authors place of work: Regionální centrum aplikované molekulární onkologie, Masarykův onkologický ústav, Brno 1;  Klinika komplexní onkologické péče, Masarykův onkologický ústav, Brno 2
Published in the journal: Klin Onkol 2018; 31(Supplementum 2): 77-81
Category: Review
doi: https://doi.org/10.14735/amko20182S77

Summary

Background:

Non-steroidal anti-inflammatory drugs (NSAID) represent a group of medicaments inhibiting cyclooxygenase (COX) enzyme, and, in parallel, these drugs show also analgesic, antipyretic and anti-inflammatory effects. Due to their efficiency, good tolerance and easy availability, they belong to the world‘s most used drugs. For decades, evidence of their anti-tumor activity has been growing, with the largest amount of published work being related to colorectal cancer (CRC). Based on both in vitro and in vivo experiments and data obtained from epidemiological and clinical studies, potential application of NSAID as chemo-preventive treatment for CRC patients is recently discussed in order to prevent development or recurrence of precanceroses and tumors. Promising treatment for such indication would be acetylsalicylic acid (ASA), which is the oldest, more than 100 years used member of the NSAID family. Nonselective irreversible COX inhibition is an important but probably not solely mechanism of its anticancer activity. Notably, wider use of ASA in chemoprevention is also prevented due to particular concerns about gastrointestinal and renal toxicity caused especially by its long-term use.

Aims:

This review introduces the role of COX in tumor biology of CRC and highlights the results of the most interesting experiments illustrating the anti-tumor effect of ASA. Moreover, our work evaluates the most important published clinical analyzes of the ASA chemopreventive effect on CRC and discusses the current state.

Key words:

non-steroidal anti-inflammatory agents – acetylsalicylic acid – colorectal carcinoma – cyclooxygenase – chemoprevention

This work was supported by the projects MEYS – NPS I – LO1413, MH CZ – DRO (MMCI, 00209805) and by Czech Science Foundation project no. 16-14829S.

The authors declare they have no potential conflicts of interest concerning drugs, products, or services used in the study.

The Editorial Board declares that the manuscript met the ICMJE recommendation for biomedical papers.

Accepted: 10. 9. 2017


Zdroje

1. Arnold M, Sierra MS, Laversanne M et al. Global patterns and trends in colorectal cancer incidence and mortality. Gut 2017; 66 (4): 683–691. doi: 10.1136/gutjnl-2015-310912.

2. Ferlay J, Steliarova-Foucher E, Lortet-Tieulent J et al. Cancer incidence and mortality patterns in Europe: estimates for 40 countries in 2012. Eur J Cancer 2013; 49 (6): 1374–1403. doi: 10.1016/j.ejca.2012.12.027.

3. Sancho E, Batlle E, Clevers H. Signaling pathways in intestinal development and cancer. Annu Rev Cell Dev Biol 2004; 20: 695–723. doi: 10.1146/annurev.cellbio.20.010403.092805.

4. Long AG, Lundsmith ET, Hamilton KE. Inflammation and colorectal cancer. Curr Colorectal Cancer Rep 2017; 13 (4): 341–351. doi: 10.1007/s11888-017-0373-6.

5. Eberhart CE, Coffey RJ, Radhika A et al. Up-regulation of cyclooxygenase 2 gene expression in human colorectal adenomas and adenocarcinomas. Gastroenterology 1994; 107 (4): 1183–1188.

6. Soslow RA, Dannenberg AJ, Rush D et al. COX-2 is expressed in human pulmonary, colonic, and mammary tumors. Cancer 2000; 89 (12): 2637–2645.

7. Brock TG, McNish RW, Peters-Golden M. Arachidonic acid is preferentially metabolized by cyclooxygenase-2 to prostacyclin and prostaglandin E2. J Biol Chem 1999; 274 (17): 11660–11666.

8. Pugh S, Thomas GA. Patients with adenomatous polyps and carcinomas have increased colonic mucosal prostaglandin E2. Gut 1994; 35 (5): 675–678.

9. Sugimoto Y, Narumiya S. Prostaglandin E receptors. J Biol Chem 2007; 282 (16): 11613–11617. doi: 10.1074/jbc.R600038200.

10. Sheng HM, Shao JY, Morrow JD et al. Modulation of apoptosis and Bcl-2 expression by prostaglandin E-2 in human colon cancer cells. Cancer Res 1998; 58 (2): 362–366.

11. Pai R, Soreghan B, Szabo IL et al. Prostaglandin E-2 transactivates EGF receptor: a novel mechanism for promoting colon cancer growth and gastrointestinal hypertrophy. Nat Med 2002; 8 (3): 289–293. doi: 10.1038/nm0302-289.

12. Castellone MD, Teramoto H, Williams BO et al. Prostaglandin E-2 promotes colon cancer cell growth through a G (s) -axin-beta-catenin signaling axis. Science 2005; 310 (5753): 1504–1510. doi: 10.1126/science.1116221.

13. Sheng H, Shao J, Washington MK et al. Prostaglandin E2 increases growth and motility of colorectal carcinoma cells. J Biol Chem 2001; 276 (21): 18075–18081. doi: 10.1074/jbc.M009689200.

14. Fukuda R, Kelly B, Semenza GL. Vascular endothelial growth factor gene expression in colon cancer cells exposed to prostaglandin E-2 is mediated by hypoxia-inducible factor 1. Cancer Res 2003; 63 (9): 2330–2334.

15. Liu B, Qu L, Yan S. Cyclooxygenase-2 promotes tumor growth and suppresses tumor immunity. Cancer Cell Int 2015; 15: 106. doi: 10.1186/s12935-015-0260-7.

16. Masunaga R, Kohno H, Dhar DK et al. Cyclooxygenase-2 expression correlates with tumor neovascularization and prognosis in human colorectal carcinoma patients. Clin Cancer Res 2000; 6 (10): 4064–4068.

17. Tomozawa S, Tsuno NH, Sunami E et al. Cyclooxygenase-2 overexpression correlates with tumour recurrence, especially haematogenous metastasis, of colorectal cancer. Br J Cancer 2000; 83 (3): 324–328. doi: 10.1054/bjoc.2000.1270.

18. Dubois RN, Abramson SB, Crofford L et al. Cyclo-oxygenase in biology and disease. FASEB J 1998; 12 (12): 1063–1073.

19. Antman EM. Evaluating the cardiovascular safety of nonsteroidal anti-inflammatory drugs. Circulation 2017; 135 (21): 2062–2072. doi: 10.1161/CIRCULATIONAHA.117.027288.

20. Waddell WR, Loughry RW. Sulindac for polyposis of the colon. J Surg Oncol 1983; 24 (1): 83–87.

21. Maier TJ, Schilling K, Schmidt R et al. Cyclooxygenase-2 (COX-2) -dependent and -independent anticarcinogenic effects of celecoxib in human colon carcinoma cells. Biochem Pharmacol 2004; 67 (8): 1469–1478. doi: 10.1016/j.bcp.2003.12.014.

22. Arico S, Pattingre S, Bauvy C et al. xxib induces apoptosis by inhibiting 3-phosphoinositide-dependent protein kinase-1 activity in the human colon cancer HT-29 cell line. J Biol Chem 2002; 277 (31): 27613–27621. doi: 10.1074/jbc.M201119200.

23. Gu M, Nishihara R, Chen Y et al. Aspirin exerts high anti-cancer activity in PIK3CA-mutant colon cancer cells. Oncotarget 2017; 8 (50): 87379–87389. doi: 10.18632/oncotarget.20972.

24. Goel A, Chang DK, Ricciardiello L et al. A novel mechanism for aspirin-mediated growth inhibition of human colon cancer cells. Clin Cancer Res 2003; 9 (1): 383–390.

25. Piqué M, Barragán M, Dalmau M et al. Aspirin induces apoptosis through mitochondrial cytochrome c release. FEBS Lett 2000; 480 (2–3): 193–196.

26. Dihlmann S, Siermann A, von Knebel Doeberitz M. The nonsteroidal anti-inflammatory drugs aspirin and indomethacin attenuate β-catenin/TCF-4 signaling. Oncogene 2001; 20 (5): 645–653. doi: 10.1038/sj.onc.1204 123.

27. Baron JA, Cole BF, Sandler RS et al. A randomized trial of aspirin to prevent colorectal adenomas. N Engl J Med 2003; 348 (10): 891–899. doi: 10.1056/NEJMoa021735.

28. Benamouzig R, Uzzan B, Deyra J et al. Prevention by daily soluble aspirin of colorectal adenoma recurrence: 4-year results of the APACC randomised trial. Gut 2012; 61 (2): 255–261. doi: 10.1136/gutjnl-2011-300113.

29. Rothwell PM, Wilson M, Elwin C-E et al. Long-term effect of aspirin on colorectal cancer incidence and mortality: 20-year follow-up of five randomised trials. Lancet 2010; 376 (9754): 1741–1750. doi: 10.1016/S0140-6736 (10) 61543-7.

30. Bibbins-Domingo K. Aspirin use for the primary prevention of cardiovascular disease and colorectal cancer: U.S. preventive services task force recommendation statement. Ann Intern Med 2016; 164 (12): 836–845. doi: 10.7326/M16-0577.

31. Burn J, Bishop DT, Chapman PD et al. A randomized placebo-controlled prevention trial of aspirin and/or resistant starch in young people with familial adenomatous polyposis. Cancer Prev Res (Phila) 2011; 4 (5): 655–665. doi: 10.1158/1940-6207.CAPR-11-0106.

32. Burn J, Gerdes A-M, Macrae F et al. Long-term effect of aspirin on cancer risk in carriers of hereditary colorectal cancer: an analysis from the CAPP2 randomised controlled trial. Lancet 2011; 378 (9809): 2081–2087. doi: 10.1016/S0140-6736 (11) 61049-0.

33. Gray RT, Coleman HG, Hughes C et al. Low-dose aspirin use and survival in colorectal cancer: results from a population-based cohort study. BMC Cancer 2018; 18 (1): 228. doi: 10.1186/s12885-018-4142-y.

34. clinicaltrials.gov. [online]. Available from: https: //clinicaltrials.gov/.

35. Chan AT, Ogino S, Fuchs CS. Aspirin and the risk of colorectal cancer in relation to the expression of COX-2.  N Engl J Med 2007; 356 (21): 2131–2142. doi: 10.1056/NEJMoa067208.

36. Liao X, Lochhead P, Nishihara R et al. Aspirin use, tumor PIK3CA mutation, and colorectal-cancer survival. N Engl J Med 2012; 367 (17): 1596–1606. doi: 10.1056/NEJMoa1207756.

Štítky
Paediatric clinical oncology Surgery Clinical oncology

Článok vyšiel v časopise

Clinical Oncology

Číslo Supplementum 2

2018 Číslo Supplementum 2
Najčítanejšie tento týždeň
Najčítanejšie v tomto čísle
Prihlásenie
Zabudnuté heslo

Zadajte e-mailovú adresu, s ktorou ste vytvárali účet. Budú Vám na ňu zasielané informácie k nastaveniu nového hesla.

Prihlásenie

Nemáte účet?  Registrujte sa

#ADS_BOTTOM_SCRIPTS#