Notch signal pathway is an important mediator of growth and survival in several cancer types, while Notch pathway genes function as oncogenes or tumor suppressors in different cancers. Although aberrant Notch activation contributes to leukemogenesis in T cells, the role of Notch pathway in acute myeloid leukemia (AML) remains unclear. To address this problem, we investigated the expression levels of its downstream effector Hes1 and p21 in primary AML cells and cell lines by realtime PCR and western, and found that both of them was weak in these cells. Induced activation of Hes1 consisently led to AML growth arrest and apoptosis, which was associated with enhanced p21 expression. Besides, overexpression of Hes1 inhibited growth of AML cells in vivo. In conclusion, we reported that Hes1 mediated growth arrest and apoptosis of human AML cells, and demonstrated a novel tumor suppressor role for Hes1 in AML.

Disclosures

No relevant conflicts of interest to declare.

Topics:
apoptosis, cancer, cell lines, conflict of interest, disclosure, genes, leukemia, myelocytic, acute, leukemogenesis, oncogenes, polymerase chain reaction

Author notes

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Asterisk with author names denotes non-ASH members.

© 2014 by The American Society of Hematology
2014
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