Abstract
The Notch signaling pathway plays a critical role in maintaining the balance between cell proliferation, differentiation and apoptosis, and is a highly conserved signaling pathway that regulates normal development in a context- and dose-dependent manner. Dysregulation of Notch signaling has been suggested to be key events in a variety of hematological malignancies. Notch1 signaling appears to be the central oncogenic trigger in T cell acute lymphoblastic leukemia (T-ALL), in which the majority of human malignancies have acquired mutations that lead to constitutive activation of Notch1 signaling. However, emerging evidence unexpectedly demonstrates that Notch signaling can function as a potent tumor suppressor in other forms of leukemia. This minireview will summarize recent advances related to the roles of activated Notch signaling in human lymphocytic leukemia, myeloid leukemia, stem cells and stromal microenvironment, and we will discuss the perspectives of Notch signaling as a potential therapeutic target as well.
Highlights
The Notch signaling pathway is highly conserved from Drosophila to human and plays an important role in the regulation of cell proliferation, differentiation and apoptosis [1]
A significant decrease in the levels of the Notch ligand and activated receptors as well as target genes was reported to be lower in acute myeloid leukemia (AML) samples than in normal hematopoietic stem cells (HSCs), suggesting that Notch signaling is not activated in AML [46,47,48]
Kannan et al have found that all four Notch homologues and Hes1 were sufficient to inhibit the growth and induced caspase-dependent apoptosis of AML, which were associated with B cell lymphoma 2 (BCL2) loss and enhanced p53/p21 expression [45]
Summary
The Notch signaling pathway is highly conserved from Drosophila to human and plays an important role in the regulation of cell proliferation, differentiation and apoptosis [1]. Introduction The Notch signaling pathway is highly conserved from Drosophila to human and plays an important role in the regulation of cell proliferation, differentiation and apoptosis [1]. Downregulation of Notch3 by small hair RNA (shRNA) has been found to suppress the activity of Notch signaling, leading to growth inhibition and apoptosis induction of T-ALL cells [32].
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