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2017 ; 7
(ä): 54
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Transcription Factor GFI1B in Health and Disease
#MMPMID28401061
Anguita E
; Candel FJ
; Chaparro A
; Roldán-Etcheverry JJ
Front Oncol
2017[]; 7
(ä): 54
PMID28401061
show ga
Many human diseases arise through dysregulation of genes that control key cell
fate pathways. Transcription factors (TFs) are major cell fate regulators
frequently involved in cancer, particularly in leukemia. The GFI1B gene, coding a
TF, was identified by sequence homology with the oncogene growth factor
independence 1 (GFI1). Both GFI1 and GFI1B have six C-terminal C2H2 zinc fingers
and an N-terminal SNAG (SNAIL/GFI1) transcriptional repression domain. Gfi1 is
essential for neutrophil differentiation in mice. In humans, GFI1 mutations are
associated with severe congenital neutropenia. Gfi1 is also required for B and T
lymphopoiesis. However, knockout mice have demonstrated that Gfi1b is required
for development of both erythroid and megakaryocytic lineages. Consistent with
this, human mutations of GFI1B produce bleeding disorders with low platelet count
and abnormal function. Loss of Gfi1b in adult mice increases the absolute numbers
of hematopoietic stem cells (HSCs) that are less quiescent than wild-type HSCs.
In keeping with this key role in cell fate, GFI1B is emerging as a gene involved
in cancer, which also includes solid tumors. In fact, abnormal activation of
GFI1B and GFI1 has been related to human medulloblastoma and is also likely to be
relevant in blood malignancies. Several pieces of evidence supporting this
statement will be detailed in this mini review.
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