Antiproliferative effect of trichostatin A and HC-toxin in T47D human breast cancer cells

Archives of Pharmacal Research

Volumn 27, Issue 6, 2004, Pages 640-645

  Ki, Eun Joung ^a   Kim, Dae Kee ^a   Sheen, Yhun Yhong ^a  

^a Ewha Womans University   (South Korea)

Author keywords

HC toxin; Histone deacetylase; T47D cell; Trichostatin A

Indexed keywords

ANTINEOPLASTIC AGENT; CASP3 PROTEIN, HUMAN; CASP7 PROTEIN, HUMAN; CASPASE; CASPASE 3; CASPASE 7; CYCLOPEPTIDE; HC TOXIN; HISTONE DEACETYLASE; HYDROXAMIC ACID; TOXIN; TRICHOSTATIN A;

APOPTOSIS; ARTICLE; BIOSYNTHESIS; BREAST TUMOR; CELL PROLIFERATION; COMPARATIVE STUDY; DOSE RESPONSE; DRUG ANTAGONISM; DRUG EFFECT; FLOW CYTOMETRY; FLUORESCENT ANTIBODY TECHNIQUE; HUMAN; TUMOR CELL LINE;

ANTINEOPLASTIC AGENTS; APOPTOSIS; BREAST NEOPLASMS; CASPASE 3; CASPASE 7; CASPASES; CELL LINE, TUMOR; CELL PROLIFERATION; DOSE-RESPONSE RELATIONSHIP, DRUG; FLOW CYTOMETRY; FLUORESCENT ANTIBODY TECHNIQUE; HISTONE DEACETYLASES; HUMANS; HYDROXAMIC ACIDS; PEPTIDES, CYCLIC; TOXINS, BIOLOGICAL;

EID: 17344366283     PISSN: 02536269     EISSN: 02536269     Source Type: Journal    
DOI: 10.1007/bf02980164     Document Type: Article

References (20)

1. Boyes, J., Byfield, P., Nakatani, Y., and Ogryzko, V., Regulation of activity of the transcription factor GATA-1 by acetylation. Nature, 396, 594-598 (1998).
2. Chang, T. H. and Szabo, E., Enhanced growth inhibition by combination differentiation therapy with ligands of peroxisome proliferator-activated receptor-γ and inhibitors of histone deacetylase in adenocarcinoma of the lung. Clin. Cancer Res., 8, 1206-1212 (2002).
3. Cohen, L. A., Maine, S., Marks, P. A., Rifkind, R. A., Desai, D., and Richon, V. M., Chemoprevention of carcinogen-induced mammary tumorigenesis by the hybrid polar cytodifferentiation agent, suberanilohydroxamic acid (SAHA). Anticancer Res., 19, 4999-5005 (1999).
4. Corry, S. and Adams, J. M., The Bcl2 family; regulators of the cellular life-o0death switch. Nat. Rev. Cancer, 2, 647-656 (2002).
5. Finnin, M. S., Donigian, J. R., Cohen, A., Richon, V. M., Rifkind, R. A., Marks, P. A., Breslow, R., and Pavletich N. P., Structures of a histone deacetylase homologue bound to the TSA and SAHA inhibitors. Nature, 401, 188-193 (1999).
6. Greenspan, P., Mayer, E. P., and Fowler, S. D., Nile red: a selective fluorescent stain for intracellular lipid droplets. J. Cell Biol., 100, 965-973 (1985).
7. Johnstone, R. W., Histone-deacetylase inhibitors: novel drugs for the treatment of cancer. Nat. Rev. Drug Discovery, 1, 287-299 (2002a).
8. Johnstone, R. W., Ruefli, A. A., and Lowe, S. W., Apoptosis: a link between cancer fenetics and chemotherapy. Cell, 108, 153-164 (2002b).
9. Juan, L. J., Shia, W. J., Chen, M. H., Yang, W. M., Seto, E., Lin, Y. S., and Wu, C. W. Histone deacetylases specifically downregulate p53-dependent gene activation. J. Biol. Chem., 275, 20436-20443 (2000).
10. Kitamura, K., Hoshi, S., Koike, M., Kiyoi, H., Saito, H., and Naoe, T., Histone deacetylase inhibitor but not arsenic trioxide differentiates acute promyelocytic leukaemia cells with t (11;17) in combination with all-trans retinoic acid. Br. J. Haematol., 108, 696-702 (2000).
11. Lin, R. J., Nagy, L., Inoue, S., Shao, W., Miller, W. H., Jr. and Evans, R. M., Role of the histone deacetylase complex in acute promyelocytic leukaemia. Nature, 391, 811-814 (1998).
12. Marks, P., Rifkind, R. A., Richon, V. M., Breslow, R., Miller, T., and Kelly, W. K., Histone deacetylase and cancer: causes and therapeutics. Nat. Rev. Cancer, 1, 194-202 (2001).
13. Nusse, M., Beisker, W., Hoffmann, C., and Tarnok, A., Flow cytometric analysis of G1- and G2/M-phase subpopulations in mammalian cell nuclei using side scatter and DNA content measurements. Cytometry, 11, 813-821 (1990).
14. Rashid, S. F., Moore, J. S., Walker, E., Driver, P. M., Engel, J., Edwards, C. E., Brown, G., Uskokovic, M. R., and Campbell, M. J., Synergistic growth inhibition of prostate cancer cells by 1α, 25 dihydroxyvitamin Dinf3/inf and its 19-nor-hexafluoride analogs in combination with either sodium butyrate or trichostatin A. Oncogene, 20, 1860-1872 (2001).
15. Richon, V. M., Webb, Y., Merger, R., Sheppard, T., Jursic, B., Ngo, L., Civoli, F., Breslow, R., Rifkind, R. A. and Marks, P. A., Second generation hybrid polar compounds are potent inducers of transformed cell differentiation. Proc. Natl. Acad. Sci. U.S.A, 93, 5705-5708 (1996).
16. Ruefli, A. A., Ausserlechner, M. J., Bernhard, D., Sutton, V. R., Tainton, K. M., Kofler, R., Smyth, M. J., and Johnstone, R. W., The histone deacetylase inhibitor and chemotherapeutic agent suberoylanilide hydroxamic acid (SAHA) induces a cell-death pathway characterized by cleavage of Bid and production of reactive oxygen species. Proc. Natl. Acad. Sci., 98, 10833-10838 (2001).
17. Soto, A. M., Sonnenschein, C., Chung, K. L., Fernandes, M. F., Olea, N., and Serrano, F. O., The E-SCREEN assay as a tool to identify estrogens : an update on estrogenic environmental pollutants. Environ. Health Perspect, 103, 113-122 (1995).
18. Van Lint, C., Emiliani, S., and Verdin, E. The expression of a small fraction of cellular genes is changed in response to histone hyperacetylation. Gene Expr., 5, 245-253 (1996).
19. Vigushin, D. M., Ali, S., Pace, P. E., Mirsaidi, N., Ito, K., Adcock, I., and Coombes, R. C. Trichostatin A is a histone deacetylase inhibitor with potent antitumor activity against breast cancer in vivo. Clin. Cancer Res., 7, 971-976 (2001).
20. Yoshida, M., Horinouchi, S., and Beppu, T., Trichostatin A and trapoxin: novel chemical probes for the role of histone acetylation in chromatin structure and function. BioAssay, 17, 423-430 (1995).