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Laboratory of Cell Regulation and Carcinogenesis, DBS, National Cancer Institute, Bethesda, Maryland 20892-5055 [Y-H. I., H. T. K., C. L., D. P., S-J. K.]; Molecular Biology Institute and Johnson Comprehensive Cancer Center and Department of Pediatrics, Gwyne Hazen Cherry Memorial Laboratories, Division of Hematology/Oncology, University of California, Los Angeles, California 90024 [S. W., C. T. D.]; and Department of Pathology, Children’s and Women’s Hospital, Vancouver, British Columbia, V6H 3V4 Canada [P. H. B. S.]
Ewing sarcoma-specific chromosomal translocations fuse the EWS gene to a subset of ets transcription factor family members, most commonly the FLI1 gene and less frequently ERG, ETV1, E1A-F, or FEV. These fusion proteins are thought to act as aberrant transcription factors that bind DNA through their ets DNA binding domain. Recently, we have shown (K-B. Hahm et al., Nat. Genet., 23: 222–227, 1999) that the transforming growth factor ß (TGF-ß) type II receptor (TGF-ß RII), a putative tumor suppressor gene, is a target of the EWS-FLI1 fusion protein. Here, we also examined effects of EWS-ETV1 and EWS-ERG on expression of the TGF-ß RII gene. We show that relative to the control, NIH-3T3 cell lines stably transfected with the EWS-FLI1, EWS-ERG, or EWS-ETV1 gene fusion express reduced levels of TGF-ß RII mRNA and protein, and that these cell lines have reduced TGF-ß sensitivity. Cotransfection of these fusion genes and the TGF-ß RII promoter suppresses TGF-ß RII promoter activity and also FLI1-, ERG-, or ETV1-induced promoter activity. These results indicate that transcriptional repression of TGF-ß RII is an important target of the EWS-FLI1, EWS-ERG, or EWS-ETV1 oncogene, and that EWS-ets fusion proteins may function as dominant negative forms of ets transcription factors.
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