A novel mechanism for aspirin-mediated growth inhibition of human colon cancer cells

Clinical Cancer Research

Volumn 9, Issue 1 I, 2003, Pages 383-390

  Goel, Ajay ^a   Chang, Dong Kyung ^a   Ricciardiello, Luigi ^a   Gasche, Christoph ^a   Boland, C Richard ^a,b  

^a UNIVERSITY OF CALIFORNIA SAN DIEGO   (United States)

^b VA SAN DIEGO HEALTHCARE SYSTEM   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

ACETYLSALICYLIC ACID; DNA MISMATCH REPAIR PROTEIN; NONSTEROID ANTIINFLAMMATORY AGENT; PROSTAGLANDIN SYNTHASE; PROTEIN; UNCLASSIFIED DRUG;

APOPTOSIS; ARTICLE; CANCER CELL CULTURE; CANCER GROWTH; CANCER INHIBITION; CELL CYCLE; CHEMOPROPHYLAXIS; COLON CANCER; CONTROLLED STUDY; DRUG MECHANISM; DRUG TARGETING; ENZYME ACTIVITY; ENZYME INHIBITION; HUMAN; HUMAN CELL; MICROSATELLITE INSTABILITY; PRIORITY JOURNAL; PROTEIN BLOOD LEVEL; PROTEIN EXPRESSION; PROTEIN TARGETING;

ANTI-INFLAMMATORY AGENTS, NON-STEROIDAL; APOPTOSIS; ASPIRIN; BLOTTING, WESTERN; CELL CYCLE; CELL DIVISION; COLONIC NEOPLASMS; COLORING AGENTS; DNA-BINDING PROTEINS; DOSE-RESPONSE RELATIONSHIP, DRUG; G0 PHASE; G1 PHASE; HUMANS; REVERSE TRANSCRIPTASE POLYMERASE CHAIN REACTION; TETRAZOLIUM SALTS; THIAZOLES; TIME FACTORS; TUMOR CELLS, CULTURED;

EID: 0037239781     PISSN: 10780432     EISSN: None     Source Type: Journal    
DOI: None     Document Type: Article

References (38)

1. Gupta, R. A., and DuBois, R. N. Aspirin. NSAIDS, and colon cancer prevention: mechanisms? Gastroenterology, 114: 1095-1098, 1998.
2. Barnes, C. J., and Lee, M. Chemoprevention of spontaneous intestinal adenomas in the adenomatous polyposis coli Min mouse model with aspirin. Gastroenterology, 114: 873-877, 1998.
3. Lefort, J., and Vargaftig, B. B. Salicylic acid prevents inhibition by aspirin of arachidonic acid- induced hypotension, bronchoconstriction and thrombocytopenia. Br. J. Pharmacol., 60: 292P-293P, 1977.
4. Humes, J. L., Winter, C. A., Sadowski, S. J., and Kuehl, F. A., Jr. Multiple sites on prostaglandin cyclooxygenase are determinants in the action of nonsteroidal antiinflammatory agents. Proc. Natl. Acad. Sci. USA, 78: 2053-2056, 1981.
5. Hanif, R., Pittas, A., Feng, Y., Koutsos, M. I., Qiao, L., Staiano-Coico, L., Shiff, S. I., and Rigas, B. Effects of nonsteroidal anti-inflammatory drugs on proliferation and on induction of apoptosis in colon cancer cells by a prostaglandin-independent pathway. Biochem. Pharmacol., 52: 237-245, 1996.
6. Zhang, X., Morham, S. G., Langenbach, R., and Young, D. A. Malignant transformation and antineoplastic actions of nonsteroidal antiinflammatory drugs (NSAIDs) on cyclooxygenase-null embryo fibroblasts. J. Exp. Med., 190: 451-459, 1999.
7. Biemond, P., Swaak, A. J., Penders, J. M., Beindorff, C. M., and Koster, J. F. Superoxide production by polymorphonuclear leucocytes in rheumatoid arthritis and osteoarthritis: in vivo inhibition by the anti-rheumatic drug piroxicam due to interference with the activation of the NADPH- oxidase. Ann. Rheum. Dis., 45: 249-255, 1986.
8. Shiff, S. J., and Rigas, B. Nonsteroidal anti-inflammatory drugs and colorectal cancer: evolving concepts of their chemopreventive actions. Gastroenterology, 113: 1992-1998, 1997.
9. Kopp, E., and Ghosh, S. Inhibition of NF-kappa B by sodium salicylate and aspirin. Science (Wash. DC), 265: 956-959, 1994.
10. Stark, L. A., Din, F. V., Zwacka, R. M., and Dunlop, M. G. Aspirin-induced activation of the NF-κB signaling pathway: a novel mechanism for aspirin-mediated apoptosis in colon cancer cells. FASEB J., 15: 1273-1275, 2001.
11. Schwenger, P., Bellosta, P., Vietor, I., Basilico, C., Skolnik, E. Y., and Vilcek, J. Sodium salicylate induces apoptosis via p38 mitogen-activated protein kinase but inhibits tumor necrosis factor-induced c-Jun N-terminal kinase/stress-activated protein kinase activation. Proc. Natl. Acad. Sci. USA, 94: 2869-2873, 1997.
12. Lehmann, J. M., Lenhard, J. M., Oliver, B. B., Ringold, G. M., and Kliewer, S. A. Peroxisome proliferator-activated receptors α and γ are activated by indomethacin and other non-steroidal anti-inflammatory drugs. J. Biol. Chem., 272: 3406-3410, 1997.
13. Ruschoff, J., Wallinger, S., Dietmaier, W., Bocker, T., Brockhoff, G., Hofstadter, F., and Fishel, R. Aspirin suppresses the mutator phenotype associated with hereditary nonpolyposis colorectal cancer by genetic selection. Proc. Natl. Acad. Sci. USA, 95: 11301-11306. 1998.
14. Boyer, J. C., Umar, A., Risinger, J. I., Lipford, J. R., Kane, M., Yin, S., Barrett, J. C., Kolodner, R. D., and Kunkel, T. A. Microsatellite instability, mismatch repair deficiency, and genetic defects in human cancer cell lines. Cancer Res., 55: 6063-6070, 1995.
15. Koi, M., Umar, A., Chauhan, D. P., Cherian, S. P., Carethers, J. M., Kunkel, T. A., and Boland, C. R. Human chromosome 3 corrects mismatch repair deficiency and microsatellite instability and reduces N-methyl-N′-nitro-N- nitrosoguanidine tolerance in colon tumor cells with homozygous hMLH1 mutation (Published erratum appears in Cancer Res., 55: 201, 1995). Cancer Res., 54: 4308-4312, 1994.
16. Ealey, P. A., Yateman, M. E., Sandhu, R., Dattani, M. T., Hassan, M. K., Holt, S. J., and Marshall, N. J. The development of an eluted stain bioassay (ESTA) for human growth hormone. Growth Regul., 5: 36-44, 1995.
17. Marra, G., Chang, C. L., Laghi, L. A., Chauhan, D. P., Young, D., and Boland, C. R. Expression of human MutS homolog 2 (hMSH2) protein in resting and proliferating cells. Oncogene, 13: 2189-2196, 1996.
18. Chang, D. K., Ricciardiello, L., Goel, A., Chang, C. L., and Boland, C. R. Steady-state regulation of the human DNA mismatch repair system. J. Biol. Chem., 275: 18424-18431, 2000.
19. Vindelov, L. L., and Christensen, I. J. A review of techniques and results obtained in one laboratory by an integrated system of methods designed for routine clinical flow cytometric DNA analysis. Cytometry, 11: 753-770, 1990.
20. DuBois, R. N., Giardiello, F. M., and Smalley, W. E. Nonsteroidal anti-inflammatory drugs, eicosanoids, and colorectal cancer prevention. Gastroenterol. Clin. N. Am., 25: 773-791, 1996.
21. Lee, I. M., Hennekens, C. H., and Buring, J. E. Use of aspirin and other nonsteroidal antiinflammatory drugs and the risk of cancer development. In: V. T. DeVita, S. Hellman, and S. A. Rosenberg (eds.), Cancer: Principles and Practice of Oncology, pp. 599-607. Philadelphia, PA: Lippincott-Raven, 1997.
22. Marnett, L. J. Generation of mutagens during arachidonic acid metabolism. Cancer Metastasis Rev., 13: 303-308, 1994.
23. Young, M. R. Eicosanoids and the immunology of cancer. Cancer Metastasis Rev., 13: 337-348, 1994.
24. Abramson, S. B., Leszczynska-Piziak, J., Haines, K., and Reibman, J. Non-steroidal anti-inflammatory drugs: effects on a GTP binding protein within the neutrophil plasma membrane. Biochem. Pharmacol., 41: 1567-1573, 1991.
25. Abramson, S., Korchak, H., Ludewig, R., Edelson, H., Haines, K., Levin, R. I., Herman, R., Rider, L., Kimmel, S., and Weissmann, G. Modes of action of aspirin-like drugs. Proc. Natl. Acad. Sci. USA, 82: 7227-7231, 1985.
26. Hixson, L. J., Alberts, D. S., Krutzsch, M., Einsphar, J., Brendel, K., Gross, P. H., Paranka, N. S., Baier, M., Emerson, S., and Pamukcu, R. Antiproliferative effect of nonsteroidal antiinflammatory drugs against human colon cancer cells. Cancer Epidemiol. Biomark. Prev., 3: 433-438, 1994.
27. Marra, G., and Boland, C. R. DNA repair and colorectal cancer. Gastroenterol. Clin. N. Am., 25: 755-772, 1996.
28. Mellon, I., Rajpal, D. K., Koi, M., Boland, C. R., and Champe, G. N. Transcription-coupled repair deficiency and mutations in human mismatch repair genes. Science (Wash. DC), 272: 557-560, 1996.
29. Mellon, I., and Champe, G. N. Products of DNA mismatch repair genes mutS and mutL are required for transcription-coupled nucleotide-excision repair of the lactose operon in Escherichia coli. Proc. Natl. Acad. Sci. USA. 93: 1292-1297, 1996.
30. 2 cell cycle checkpoint. Cancer Res., 55: 3721-3725, 1995.
31. Carethers, J. M., Hawn, M. T., Chauhan, D. P., Luce, M. C., Marra, G., Koi, M., and Boland, C. R. Competency in mismatch repair prohibits clonal expansion of cancer cells treated with N-methyl-N′-nitro-N-nitrosoguanidine. J. Clin. Investig., 98: 199-206, 1996.
32. Zhang, H., Richards, B., Wilson, T., Lloyd, M., Cranston, A., Thorburn, A., Fishel, R., and Meuth, M. Apoptosis induced by overexpression of hMSH2 or hMLH1. Cancer Res., 59: 3021-3027, 1999.
33. Elder, D. J., Hague, A., Hicks, D. J., and Paraskeva, C. Differential growth inhibition by the aspirin metabolite salicylate in human colorectal tumor cell lines: enhanced apoptosis in carcinoma and in vitro-transformed adenoma relative to adenoma relative to adenoma cell lines. Cancer Res., 56: 2273-2276, 1996.
34. Pasricha, P. J., Bedi, A., O'Connor, K., Rashid, A., Akhtar, A. J., Zahurak, M. L., Piantadosi, S., Hamilton, S. R., and Giardiello, F. M. The effects of sulindac on colorectal proliferation and apoptosis in familial adenomatous polyposis. Gastroenterology, 109: 994-998, 1995.
35. Subbegowda, R., and Frommel, T. O. Aspirin toxicity for human colonic tumor cells results from necrosis and is accompanied by cell cycle arrest. Cancer Res., 58: 2772-2776, 1998.
36. Shiff, S. J., Koutsos, M. I., Qiao, L., and Rigas, B. Nonsteroidal antiinflammatory drugs inhibit the proliferation of colon adenocarcinoma cells: effects on cell cycle and apoptosis. Exp. Cell Res., 222: 179-188, 1996.
37. Pachman, L. M., Olufs, R., Procknal, J. A., and Levy, G. Pharmacokinetic monitoring of salicylate therapy in children with juvenile rheumatoid arthritis. Arthritis Rheum., 22: 826-831, 1979.
38. Paulus, H. E., Siegel, M., Mongan, E., Okun, R., and Calabro, J. J. Variations of serum concentrations and half-life of salicylate in patients with rheumatoid arthritis. Arthritis Rheum., 14: 527-532, 1971.