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[Cancer Research 61, 931-934, February 1, 2001]
© 2001 American Association for Cancer Research

Advances in Brief

MS-275, A Histone Deacetylase Inhibitor, Selectively Induces Transforming Growth Factor ß Type II Receptor Expression in Human Breast Cancer Cells

Byoung Ick Lee1, Seok Hee Park1, Jin Woo Kim, Edward A. Sausville, Heung Tae Kim, Osamu Nakanishi, Jane B. Trepel and Seong-Jin Kim2

Laboratory of Cell Regulation and Carcinogenesis [B. I. L., S. H. P., H. T. K., S-J. K.], Developmental Therapeutics Program [E. A. S.], and the Medicine Branch [J. W. K., J. B. T.], National Cancer Institute, Bethesda, Maryland 20892, and Mitsui Pharmaceuticals, Chiba 297-0017, Japan [O. N.]

Transcriptional repression of the transforming growth factor (TGF)-ß type II receptor (TßRII) gene appears to be a major mechanism to inactivate TGF-ß responsiveness in many human cancers. Because histone acetylation/deacetylation plays a role in transcriptional regulation, we have examined the effect of MS-275, a synthetic inhibitor of histone deacetylase, in human breast cancer cell lines. MS-275 showed antiproliferative activity against all human breast cancer cell lines examined and induced TßRII mRNA, but not TGF-ß type I receptor mRNA. MS-275 caused an accumulation of acetylated histones H3 and H4 in total cellular chromatin. An increase in the accumulation of acetylated histones H3 and H4 was detected in the TßRII promoter after treatment with MS-275. However, the level of histone acetylation did not change in chromatin associated with the TGF-ß type I receptor gene. MS-275 treatment enhanced TGF-ß1-induced plasminogen activator inhibitor 1 expression. Thus, antitumor activity of MS-275 may be mediated in part through the induction of TßRII expression and consequent potentiation of TGF-ß signaling.




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