The role of Fli-1 in normal cell function and malignant transformation.
Aberrant 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.
Truong
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AH
Division of Cancer Biology Research, Sunnybrook and Women's College Health Sciences Centre & Toronto-Sunnybrook Regional Cancer Centre (TSRCC), 2075 Bayview Avenue, S-Wing, Room S216, Toronto, Ontario, Canada M4N 3M5.
Ben-David
Y
Y
D016475:3T3 Cells; D000328:Adult; D000818:Animals; D017209:Apoptosis / Q000235:genetics; D001859:Bone Neoplasms / Q000235:genetics; D002454:Cell Differentiation / Q000235:genetics; D002471:Cell Transformation, Neoplastic / Q000235:genetics / Q000378:metabolism*; D002472:Cell Transformation, Viral / Q000235:genetics; D004247:DNA / Q000378:metabolism; D004268:DNA-Binding Proteins / Q000235:genetics / Q000502:physiology*; D005622:Friend murine leukemia virus / Q000235:genetics; D020440:Gene Duplication; D005786:Gene Expression Regulation; D015972:Gene Expression Regulation, Neoplastic; D018257:Helix-Loop-Helix Motifs; D006410:Hematopoiesis / Q000235:genetics; D006801:Humans; D004915:Leukemia, Erythroblastic, Acute / Q000235:genetics / Q000821:virology; D051379:Mice; D018345:Mice, Knockout; D005810:Multigene Family; D009363:Neoplasm Proteins / Q000235:genetics / Q000502:physiology; D015513:Oncogene Proteins / Q000378:metabolism; D015514:Oncogene Proteins, Fusion / Q000235:genetics / Q000502:physiology; D009928:Organ Specificity; D011401:Promoter Regions, Genetic; D011485:Protein Binding; D017434:Protein Structure, Tertiary; D051789:Proto-Oncogene Protein c-fli-1; D011518:Proto-Oncogene Proteins; D034802:RNA-Binding Protein EWS; D012512:Sarcoma, Ewing / Q000235:genetics; D017384:Sequence Deletion; D015534:Trans-Activators / Q000235:genetics / Q000502:physiology*; D014157:Transcription Factors / Q000235:genetics / Q000502:physiology
D004268:DNA-Binding Proteins; C106031:EWS-FLI fusion protein; C497426:Fli1 protein, mouse; D009363:Neoplasm Proteins; D015513:Oncogene Proteins; D015514:Oncogene Proteins, Fusion; D051789:Proto-Oncogene Protein c-fli-1; D011518:Proto-Oncogene Proteins; D034802:RNA-Binding Protein EWS; D015534:Trans-Activators; D014157:Transcription Factors; D004247:DNA