Retinyl methyl ether down-regulates activator protein 1 transcriptional activation in breast cancer cells

Cancer Research

Volumn 57, Issue 16, 1997, Pages 3444-3450

  Agadir, Anissa ^a   Shealy, Y Fulmer ^b   Hill, Donald L ^b   Zhang, Xiao Kun ^a  

^a BURNHAM INSTITUTE   (United States)

^b SOUTHERN RESEARCH INSTITUTE   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

CELL NUCLEUS RECEPTOR; GROWTH FACTOR; INSULIN; PHORBOL 13 ACETATE 12 MYRISTATE; RETINOIC ACID; RETINOID; RETINOID X RECEPTOR; RETINOL METHYL ETHER; SYNAPSIN I; TRANSCRIPTION FACTOR; TRANSCRIPTION FACTOR AP 1;

ANTINEOPLASTIC ACTIVITY; ARTICLE; BINDING SITE; BREAST CANCER; CANCER CELL; DOWN REGULATION; GENE REPRESSION; GENETIC TRANSCRIPTION; HUMAN; HUMAN CELL; ONCOGENE C FOS; PRIORITY JOURNAL; PROMOTER REGION; TRANSCRIPTION REGULATION;

BREAST NEOPLASMS; CARCINOGENS; COLLAGENASES; DNA-BINDING PROTEINS; DOWN-REGULATION; ENZYME ACTIVATION; EPIDERMAL GROWTH FACTOR; GENES, REPORTER; HELA CELLS; HUMANS; PROTO-ONCOGENE PROTEINS C-FOS; PROTO-ONCOGENE PROTEINS C-JUN; RECEPTORS, RETINOIC ACID; RETINOID X RECEPTORS; TETRADECANOYLPHORBOL ACETATE; TRANS-ACTIVATION (GENETICS); TRANSCRIPTION FACTOR AP-1; TRANSCRIPTION FACTORS; TRANSFECTION; TUMOR CELLS, CULTURED; VITAMIN A;

EID: 0030873519     PISSN: 00085472     EISSN: None     Source Type: Journal    
DOI: None     Document Type: Article

References (41)

1. Lotan, R. Effect of vitamin A and its analogs (retinoids) on normal and neoplastic cells. Biochim. Biophys. Acta, 605: 33-91, 1981.
2. Gudas, L. J., Sporn, M. B., and Roberts, A. B. Cellular biology and biochemistry of the retinoids. In: M. B. Sporn, A. B. Roberts, and D. S. Goodman (eds.), The Retinoids, 2nd edition, pp. 443-520. New York: Raven Press, 1994.
3. Lippman, S. M., Kessler, J. F., and Meyskens, F. L. Retinoids as preventive and therapeutic anticancer agents. Cancer Treat. Rep., 77: 493-515, 1987.
4. Bollag, W., and Holdener, E. E. Retinoids in cancer prevention and therapy. Ann. Oncol., 3: 513-526, 1992.
5. Grubbs, C. J., Moon, R. C., Sporn, M. B., and Newton, D. L. Inhibition of mammary cancer by retinyl methyl ether. Cancer Res., 37: 599-602, 1977.
6. Hill, D. L., and Grubbs, C. J. Retinoids as chemopreventive and anticancer agents in intact animals. Anticancer Res., 2: 111-124, 1982.
7. Shealy, Y. F. Synthesis and evaluation of some new retinoids for cancer chemoprevention. Prev. Med., 18: 624-645, 1989.
8. Chopra, D. P., and Wilkoff, L. J. Reversal by vitamin A analogues (retinoids) of hyperplasia induced by N-methyl-N'-nitro-N-nitrosoguanidine in mouse prostate organ cultures. J. Natl, Cancer Inst., 58: 923-930, 1977.
9. Mossman, B. T., Craighead, J. E., and MacPherson. B. V. Asbestos-induced epithelial changes in organ cultures of hamster trachea: inhibition by retinyl methyl ether. Science (Washington DC), 207: 311-313, 1980.
10. Hill, D. L., and Sani, B. P. Metabolic disposition and development of new chemopreventive retinoids. Drug Metab. Rev., 23: 313-338, 1991.
11. Mangelsdorf, D. J., and Evans, R. M. The RXR heterodimers and orphan receptors. Cell, 83: 841-850, 1995.
12. Kastner, P., Mark, M., and Chambon, P. Nonsteroid nuclear receptors: what are genetic studies telling us about their role in real life? Cell, 83: 859-869, 1995.
13. Mangelsdorf, D. J., Thummel, C., Besto, M., Herrlich, P., Schutz, G., Umesowo, K., Blumberg, B., Kastner, P., Marle, M., Chambon, P., and Evans, R. M. The nuclear receptor superfamily: the second decade. Cell, 83: 835-839, 1995.
14. Pfahl, M. Nuclear receptor/AP-1 interaction. Endocr. Rev., 14: 651-658, 1993.
15. Warrell, R. P., Jr., de The, H., Wang, Z-Y., and Degos, L. Acute promyelocytic leukemia. N. Engl. J. Med., 329: 177-189, 1993.
16. Liu, Y., Lee, M-O., Wang, H-G., Li, Y., Hashimoto, Y., Klaus, M., Reed, J. C., and Zhang, X-k. RARβ mediates the growth inhibitory effect of retinoic acid by inducing cell apoptosis in human breast cancer cells. Mol. Cell. Biol., 16: 1138-1149, 1996.
17. Lotan, R., Xu, X-C., Lippman, S. M., Ro, J. Y., Lee, J. J., and Hong, W. K. Suppression of retinoic acid receptor β in premalignant oral lesions and its up-regulation by isotretinoin. N. Engl. J. Med., 332: 1405-1410, 1995.
18. Yang-Yen, H. F., Zhang, X-k., Graupner, G., Tzukerman, M., Sakamoto, B., Karin, M., and Pfahl, M. Antagonism between retinoic acid receptors and AP-1: implications for tumor promotion and inflammation. New Biol., 3: 1206-1219, 1991.
19. Schule, R., Rangarajan, P., Yang, N., Kliewer, S., Ransone, L. J., Bolado, J., Verma, I. M., and Evans, R. M. Retinoic acid is a negative regulator of AP-1 responsive genes. Proc. Natl. Acad. Sci. USA, 88: 6092-6096, 1991.
20. Nicholson, R., Mader, S., Nagpal, S., Leid, M., Rochette-Egly, C., and Chambon, P. Negative regulation of the rat stromelysin gene promoter by retinoic acid is mediated by an AP1 binding site. EMBO J., 9: 4443-4454, 1990.
21. Angel, P., and Karin, M. The role of Jun, Fos, and the AP-1 complex in cell proliferation and transformation. Biochim. Biophys. Acta, 1072: 129-157, 1991.
22. Kamei, Y., Xu, L., Heinzel, T., Torchia, J., Kurokawa, R., Gloss, B. Lin, S-C., Heyman, R. A., Rose, D. W., Glass, C. K., and Rosenfeld, M. G. A CBP integrator complex that mediates transcriptional activation and AP-1 inhibition by nuclear receptors. Cell, 85: 403-414, 1996.
23. Chrivia, J. C., Kwok, R. P. S., Lamb, N., Hagihara, M., Montminy, M. R., and Goodman, R. H. Phosphorylated CREB binds specifically to the nuclear protein CBP. Nature (Lond.), 365: 855-859, 1993.
24. Kwok, R. P. S., Lundblad, J. R., Chrivia, J. C., Richards, J. P., Bachinger, H. P., Brennan, R. G., Roberts, S. G., Green, M. R., and Goodman, R. H. Nuclear protein CBP is a coactivator for the transcription factor CREB. Nature (Lond.), 370: 223-226, 1994.
25. Arias, J., Alberts, A. S., Brindle, P., Claret, F. X., Smeal, T., Karin, M., Feramisco, J., and Montimony, M. Activation of cAMP and mitogen responsive genes relies on a common nuclear factor. Nature (Lond.), 370: 226-229, 1994.
26. Li, J. J., Doilg, Z., Dawson, M. I., and Colburn, N. H. Inhibition of tumor promoter-induced transformation by retinoids that transrepress AP-1 without transactivating retinoic acid response element. Cancer Res., 56: 483-489, 1996.
27. Chen, J. Y., Penco, S., Ostowski, J., Balaguer, P., Pons, M., Starrett, J. E., Reczek, P., Chambon, P., and Gronemeyer, H. RAR-specific agonist/antagonists which dissociate transactivation and AP-1 transrepression inhibit anchorage-independent cell proliferation. EMBO J., 14: 1187-1197, 1995.
28. Fanjul, A., Dawson, M. I., Hobbs, P. D., Jong, L., Cameron, J. F., Harlev, E., Graupner, G., Lu, X. P., and Pfahl, M. A new class of retinoids with selective inhibition of AP-1 inhibits proliferation. Nature (Lond.), 372: 107-111, 1994.
29. Sani, B. P., Zhang, X-k., Hill, D. L., and Shealy, Y. F. Retinyl ethers: binding properties, chemopreventive potential, and transcriptional regulation. Biochem. Biophys. Res. Commun., 223: 293-298, 1996.
30. Angel, P., Imagawa, M., Chiu, R., Stein, B., Imbra, R. J., Rahmsdorf, H. J., Jonat, C., Herrlich, P., and Karin, M. Phorbol ester-inducible genes contain a common cis element recognized by a TPA-modulated trans-acting factor. Cell, 49: 729-739, 1987.
31. Luckow, B., and Schutz, G. CAT constructions with multiple unique restriction sites for the functional analysis of eukaryotic promoters and regulatory elements. Nucleic Acids Res., 15: 5490, 1987.
32. Zhang, X-k., Hoffmann, B., Tran, P., Graupner, G., and Pfahl, M. Retinoid X receptor is an auxiliary protein for thyroid hormone and retinoic acid receptors. Nature (Lond.), 355: 441-446, 1992.
33. Lee, M-O., Liu, Y., and Zhang, X-k. A retinoic acid response element that overlaps an estrogen response element mediates multihormonal sensitivity in transcriptional activation of the lactoferrin gene. Mol. Cell. Biol., 15: 4194-4207, 1995.
34. Macaulay, V. M. Insulin-like growth factors and cancer. Br. J. Cancer, 65: 311-320, 1992.
35. Ozanne, B., Richars, C. S., Hendler, F., Burns, D., and Gusterson, B. Over-expression of the EGF receptor is a hallmark of squamous cell carcinomas. J. Pathol., 149: 9-14, 1986.
36. Salbert, G., Fanjul, A., Piedrafita, F. J., Lu, X. P., Kim, S. J., Tran, P., and Pfahl, M. Retinoic acid receptors and retinoid X receptor α down-regulate the transforming factor-β1 promoter by antagonizing AP-1 activity. Mol. Endocrinol., 7: 1347-1356, 1993.
37. Soprano, D. R., Chen, L. X., Wu, S., Donigan, A. M., Borghaei, R. C., and Soprano, K. J. Overexpression of both RAR and RXR restores AP-1 repression in adenocarcinoma cells resistant to retinoic acid-dependent growth inhibition. Oncogene, 12: 577-584, 1996.
38. Ransone, L. J., and Verma, I. M. Nuclear proto-oncogenes Fos and Jun. Annu. Rev. Cell Biol., 6: 539-557, 1990.
39. Lim, R. W., Zhu, C. Y., and Stringer, B. Differential regulation of primary response gene expression in skeletal muscle cell through multiple signal transduction pathways. Biochim. Biophys. Acta, 1266: 91-100, 1995.
40. Furcht, L. T., Skubitz, A. P., and Fields, G. B. Tumor cell invasion, matrix metallo-proteinases, and the dogma. Lab. Invest., 70: 781-783, 1994.
41. Leaman, D. W., Pisharody, S., Flickinger, T. W., Commane, M. A., Schlessinger, J., Kerr, I. M., Levy, D. E., and Stark, G. R. Roles of JAKs in activation of STATs and stimulation of c-Fos gene expression by epidermal growth factor. Mol. Cell. Biol., 16: 369-375, 1996.