Current insights into the role of Fli-1 in hematopoiesis and malignant transformation

Fli-1, a member of the ETS family of transcription factors, was discovered in 1991 through retroviral insertional mutagenesis as a driver of mouse erythroleukemias. In the past 30 years, nearly 2000 papers have defined its biology and impact on normal development and cancer. In the hematopoietic system, Fli-1 controls self-renewal of stem cells and their differentiation into diverse mature blood cells. Fli-1 also controls endothelial survival and vasculogenesis, and high and low levels of Fli-1 are implicated in the auto-immune diseases systemic lupus erythematosus and systemic sclerosis, respectively. In addition, aberrant Fli-1 expression is observed in, and is essential for, the growth of multiple hematological malignancies and solid cancers. Here, we review the historical context and latest research on Fli-1, focusing on its role in hematopoiesis, immune response, and malignant transformation. The importance of identifying Fli-1 modulators (both agonists and antagonists) and their potential clinical applications is discussed.

Automated summary

Fli-1, a member of the ETS family of transcription factors, plays a crucial role in normal development, cancer, and immune diseases. It controls the self-renewal and differentiation of stem cells in the hematopoietic system and is involved in endothelial cell survival and vasculogenesis. Aberrant Fli-1 expression is associated with various hematological and solid cancers.