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The role of Fli-1 in normal cell function and malignant transformation Truong AH; Ben-David YOncogene 2000[Dec]; 19 (55): 6482-9Aberrant expression of the Fli-1 transcription factor following genetic mutation has been recognized as a seminal event in the initiation of certain types of malignant transformation. Indeed, the etiology of a number of virally induced leukemias, including Friend virus-induced erythroleukemia, has been associated with Fli-1 overexpression. The clinical relevance of Fli-1 becomes apparent in human Ewing's sarcoma in which Fli-1 is the target of a characteristic chromosomal translocation. As such, Fli-1 has generated considerable interest over the past several years for its role in malignant transformation and tumor progression. This review will present a synopsis of the current research on Fli-1 with emphasis on its function in malignant transformation. Moreover, the possible role of Fli-1 in cellular proliferation, differentiation and survival, as well as the recent development of transgenic and knock-out mice to investigate the function of Fli-1 will be discussed. Finally, the significance of identifying target genes that are regulated by Fli-1 and their role in cellular function will be reviewed.|*Proto-Oncogene Proteins[MESH]|3T3 Cells[MESH]|Adult[MESH]|Animals[MESH]|Apoptosis/genetics[MESH]|Bone Neoplasms/genetics[MESH]|Cell Differentiation/genetics[MESH]|Cell Transformation, Neoplastic/genetics/*metabolism[MESH]|Cell Transformation, Viral/genetics[MESH]|DNA-Binding Proteins/genetics/*physiology[MESH]|DNA/metabolism[MESH]|Friend murine leukemia virus/genetics[MESH]|Gene Duplication[MESH]|Gene Expression Regulation[MESH]|Gene Expression Regulation, Neoplastic[MESH]|Helix-Loop-Helix Motifs[MESH]|Hematopoiesis/genetics[MESH]|Humans[MESH]|Leukemia, Erythroblastic, Acute/genetics/virology[MESH]|Mice[MESH]|Mice, Knockout[MESH]|Multigene Family[MESH]|Neoplasm Proteins/genetics/physiology[MESH]|Oncogene Proteins, Fusion/genetics/physiology[MESH]|Oncogene Proteins/metabolism[MESH]|Organ Specificity[MESH]|Promoter Regions, Genetic[MESH]|Protein Binding[MESH]|Protein Structure, Tertiary[MESH]|Proto-Oncogene Protein c-fli-1[MESH]|RNA-Binding Protein EWS[MESH]|Sarcoma, Ewing/genetics[MESH]|Sequence Deletion[MESH]|Trans-Activators/genetics/*physiology[MESH]|Transcription Factors/genetics/physiology[MESH] |
