Apc gene mutation is associated with a dominant-negative effect upon intestinal cell migration

Cancer Research

Volumn 57, Issue 22, 1997, Pages 5045-5050

  Mahmoud, Najjia N ^a   Boolbol, Susan K ^a,b   Bilinski, Robyn T ^a   Martucci, Charles ^b   Chadburn, Amy ^a   Bertagnolli, Monica M ^a,b  

^a WEILL CORNELL MEDICAL CENTER   (United States)

^b STRANG CANCER PREVENTION CENTER   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

BETA CATENIN; GENE PRODUCT; SULINDAC SULFIDE;

ALLELE; ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; ARTICLE; CELL ADHESION; CELL GROWTH; CELL MIGRATION; COLORECTAL CANCER; CONTROLLED STUDY; GENE MUTATION; INTESTINE CELL; MOUSE; NONHUMAN; PRIORITY JOURNAL; TUMOR SUPPRESSOR GENE;

ANALYSIS OF VARIANCE; ANIMALS; ANTI-INFLAMMATORY AGENTS, NON-STEROIDAL; APOPTOSIS; BETA CATENIN; CELL DIVISION; CELL MOVEMENT; CYTOSKELETAL PROTEINS; FEMALE; GENES, APC; INTESTINAL MUCOSA; INTESTINE, SMALL; MICE; MICE, INBRED C57BL; PROLIFERATING CELL NUCLEAR ANTIGEN; SULINDAC; TRANS-ACTIVATORS;

EID: 0030703623     PISSN: 00085472     EISSN: None     Source Type: Journal    
DOI: None     Document Type: Article

References (30)

1. Smith, K. J., Johnson, K. A., Bryan, T. M., Hill, D. E., Markowitz, S., Willson, J. V. K., Paraskeva, C., Petersen, G. M., Hamilton, S. R., Vogelstein, B., and Kinzler, K. W. The APC gene product in normal and tumor cells. Proc. Natl. Acad. Sci. USA, 90: 2846-2850, 1993.
2. Powell, S. M., Zilz, N., Beazer-Barclay, Y., Bryan, T. M., Hamilton, S. R., Thibodeau, S. N., Vogelstein, B., and Kinzler, K. W. APC mutations occur early during colorectal tumorigenesis. Nature (Lond.), 359: 235-237, 1992.
3. Kinzler, K. W., and Vogelstein, B. Lessons from hereditary colorectal cancer. Cell, 87: 159-170, 1996.
4. Peifer, M. β-Catenin as oncogene: the smoking gun. Science (Washington DC), 275: 1752-1753, 1997.
5. -/- colon carcinoma. Science (Washington DC), 275: 1784-1787, 1997.
6. Luongo, C., Moser, A. R., Gledhill, S., and Dove, W. F. Loss of APC+ in intestinal adenomas from Min mice. Cancer Res., 54: 5947-5952, 1994.
7. Oshima, M., Oshima, H., Kitagawa, K., Kohayashi, M., Itakura, C., and Taketo, M. Loss of Apc heterozygosity and abnormal tissue building in nascent intestinal polyps in mice carrying a truncated Apc gene. Proc. Natl. Acad. Sci. USA, 92: 4482-4486, 1995.
8. Boolbol, S. K., Dannenberg, A. J., Chadburn, A., Martucci, C., Guo, X-J., Ramonetti, J. T., Abreu-Goris, M., Newmark, H. L., Lipkin, M. L., DeCosse, J. J., and Bertagnolli, M. M. Cyclooxygenase-2 overexpression and tumor formation are blocked by sulindac in a murine model of familial adenomatous polyposis. Cancer Res., 56: 2556-2560, 1996.
9. Ahnen, D. J., Yoshitake, K., Kinoshita, K., and Brown, W. Proliferating cell nuclear antigen expression is a reliable marker of the proliferative compartment in the rat colon. Gastroenterology, 92: A1291, 1987.
10. Waddell, W. R., Ganser, G. F., Cerise, E. J., and Loughry, R. W. Sulindac for polyposis of the colon. Am. J. Surg., 157: 175-179, 1989.
11. Labayle, D., Fischer, D., Vielh, P., Drouhin, F., Pariente, A., Bories, C., Duhamel, O., Trousset, M., and Attali, P. Sulindac causes regression of rectal polyps in familial adenomatous polyposis. Gastroenterology, 101: 635-639, 1991.
12. Giardiello, F. M., Hamilton, S. R., Krush, A. J., et al. Treatment of colonie and rectal adenomas with sulindac in familial adenomatous polyposis. N. Engl. J. Med., 328: 1313-1316, 1993.
13. Bedi, A., Pasricha, P. J., Akhtar, A. J., Barber, J. P., Bedi, G. C., Giardiello, F. M., Zehnbauer, B. A., Hamilton, S. R., and Jones, R. J. Inhibition of apoptosis during development of colorectal cancer. Cancer Res., 55: 1811-1816, 1995.
14. Potten, C. S., Kellett, M., Rew, D. A., and Roberts, S. A. Proliferation in human gastrointestinal epithelium using bromodeoxyuridine in vivo: data for different sites, proximity to a tumour, and polyposis coli. Gut, 33: 524-529, 1992.
15. Spagnesi, M. T., Tonelli, F., Dolara, P., Caderni, G., Valanzano, R., Anastasi, A., and Bianchini, F. Rectal proliferation and polyp occurrence in patients with familial adenomatous polyposis after sulindac treatment. Gastroenterology, 106: 362-366, 1994.
16. Deschner, E. E., and Lipkin, M. Proliferative patterns in colonic mucosa in familial polyposis. Cancer (Phila.), 35: 413-418, 1975.
17. Mills, S. J., Shepherd, N. A., Hall, P. A., Hastings, A., Mathers, J. C., and Gunn, A. Proliferative compartment deregulation in the non-neoplastic colonie epithelium of familial adenomatous polyposis. Gut, 36: 391-394, 1995.
18. Li, Y. Q., Roberts, S. A., Paulus, U., Loeffler, M., and Potten, C. S. The crypt cycle in mouse small intestinal epithelium. J. Cell Sci., 107: 3271-3279, 1994.
19. Gordon, J. I. Intestinal epithelial differentiation. New insights from chimeric and transgenic mice. J. Cell. Biol., 108: 1187-1194, 1989.
20. Jankowski, J. A., Goodlad, R. A., and Wright, N. A. Maintenance of normal intestinal mucosa: function, structure, and adaptation. Gut Suppl., 1: S1-S4, 1994.
21. Przemioslo, R., Wright, N. A., Elia, G., and Ciclitira, P. J. Analysis of crypt cell proliferation in coeliac disease using MIB-1 antibody shows an increase in growth fraction. Gut, 36: 22-27, 1995.
22. Miller, J. R., and Moon, R. T. Signal transduction through beta-catenin and specification of cell fate during embryogenesis. Genes Dev., 10: 2527-2539, 1996.
23. Oyama, T., Kamai, Y., Ochiai, A., Akimoto, S., Oda, T., Yanagihara, K., Nagafuchi, A., Tsukita, S., Shibamoto, S., Ito, F., et al. A truncated beta-catenin disrupts the interaction between E-cadherin and alpha-catenin: a cause of loss of intercellular adhesiveness in human cancer cell lines. Cancer Res., 54: 6282-6287, 1994.
24. Näthke, I. S., Adams, C. L., Polakis, P., Sellin, J. H., and Nelson, W. J. The adenomatous polyposis coli tumor suppressor protein localizes to plasma membrane sites involved in active cell migration. J. Cell. Biol., 134: 165-179, 1996.
25. Earth, A. I. M., Pollack, A. L., Altschuler, Y., Su, L-K., Johnson, K. A., Smith, K. J., Hill, D. E., Vogelstein, B., and Kinzler, K. W. Association between wild type and mutant APC gene products. Cancer Res., 53: 2728-2731, 1993.
26. 2-terminal deletion of β-catenin results in stable colocalization of mutant β-catenin with adenomatous polyposis coli protein and altered MDCK cell adhesion. J. Cell. Biol., 136: 693-706, 1996.
27. Joslyn, G., Richardson, D. S., White, R., and Alber, T. Dimer formation by an N-terminal coiled coil in the APC protein. Proc. Natl. Acad. Sci. USA, 90: 11109-11113, 1993.
28. Munemitsu, S., Souza, B., Muller, O., Albert, I., Rubinfeld, B., and Polakis, P. The APC gene product associates with microtubules in vivo and promotes their assembly in vitro. Cancer Res., 54: 676-681, 1994.
29. Shoemaker, A. R., Luongo, C., Moser, A. R., Marton, L. J., and Dove, W. F. Somatic mutational mechanisms in intestinal tumor formation in Min mice. Cancer Res., 57: 1999-2006, 1997.
30. 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.