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Experimental Therapeutics |
Cell and Molecular Biology Section, Pediatric Oncology Branch [J. J., J. W., H. H., C. K., C. J. T.] and the Experimental Therapeutics Branch [R. R., S. E. B.], Center for Cancer Research, National Cancer Institute, Bethesda, Maryland 20892, and Department of Pathology, Seoul National University of Medicine, Seoul, Korea 100-799 [C. J. K.]
The antitumor efficacy of the synthetic benzamide derivative MS-27-275 (MS-275), an inhibitor of histone deacetylation [T. Suzuki et al., J. Med. Chem., 42: 3001–3003, 1999], was evaluated in a series of pediatric solid tumor cell lines, including neuroblastoma, rhabdomyosarcoma, Ewing’s sarcoma (EWS), retinoblastoma, medulloblastoma, undifferentiated sarcoma (US), osteosarcoma, and malignant rhabdoid tumors. Treatment with MS-275 results in an increase in acetylation of histones within 4 h of drug exposure. The cell lines were treated with various concentrations of MS-275 for 3 days and incubated with [3H]thymidine for 20 h before cell harvest. MS-275 inhibited [3H]thymidine uptake in a dose-dependent manner in all tumor cell lines examined. The IC50 ranged from 50 nm in the D283 medulloblastoma cell line to 1.3 µM in the US. A common feature of MS-275 treatment of pediatric tumor cell lines was induction of p21mRNA. However, the effects on cell cycle were diverse because in some cases MS-275 induced an increase in G1 or G2, whereas in others, there was an induction of apoptosis. In EWS, the EWS/fli chimeric transcription factor created by the t(11;22) suppresses transforming growth factor (TGF) ßRII transcription, however, MS-275 was able to induce an increase in TGF-ßRII mRNA and restore TGF-ß signaling. Using xenograft orthotopic models of US, EWS, and neuroblastoma, we find that the growth of established tumors is inhibited in mice treated with MS-275.
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