作者: Y Li , H Luo , T Liu , E Zacksenhaus , Y Ben-David
DOI: 10.1038/ONC.2014.162
关键词:
摘要: Friend leukemia virus-induced erythroleukemia-1 (Fli-1), an E26 transformation specific (ETS) transcription factor, was isolated a quarter century ago through retrovirus mutagenesis screen. Fli-1 has since been recognized to play critical roles in normal development and homeostasis. For example, it transcriptionally regulates genes that drive hematopoiesis vasculogenesis. Indeed, is one of 10 key regulators hematopoietic stem/progenitor cell maintenance differentiation. Aberrant expression also underlies number virally induced leukemias, including erythroleukemia various types human cancers, the target chromosomal translocations childhood Ewing's sarcoma. Abnormal important etiology autoimmune diseases such as systemic lupus erythematosus sclerosis. These studies establish strong candidate for drug development. Despite difficulties targeting factors, recent identified small-molecule inhibitors Fli-1. Here we review past ongoing research on with emphasis its mechanistic function disease malignant transformation. The significance identifying their clinical applications treatment cancer deregulated are discussed.