AKT/FOXO Signaling Enforces Reversible Differentiation Blockade in Myeloid Leukemias

نویسندگان

  • Stephen M. Sykes
  • Steven W. Lane
  • Lars Bullinger
  • Demetrios Kalaitzidis
  • Rushdia Yusuf
  • Borja Saez
  • Francesca Ferraro
  • Francois Mercier
  • Harshabad Singh
  • Kristina M. Brumme
  • Sanket S. Acharya
  • Claudia Scholl
  • Zuzana Tothova
  • Eyal C. Attar
  • Stefan Fröhling
  • Ronald A. DePinho
  • D. Gary Gilliland
  • Scott A. Armstrong
  • David T. Scadden
چکیده

AKT activation is associated with many malignancies, where AKT acts, in part, by inhibiting FOXO tumor suppressors. We show a converse role for AKT/FOXOs in acute myeloid leukemia (AML). Rather than decreased FOXO activity, we observed that FOXOs are active in ∼40% of AML patient samples regardless of genetic subtype. We also observe this activity in human MLL-AF9 leukemia allele-induced AML in mice, where either activation of Akt or compound deletion of FoxO1/3/4 reduced leukemic cell growth, with the latter markedly diminishing leukemia-initiating cell (LIC) function in vivo and improving animal survival. FOXO inhibition resulted in myeloid maturation and subsequent AML cell death. FOXO activation inversely correlated with JNK/c-JUN signaling, and leukemic cells resistant to FOXO inhibition responded to JNK inhibition. These data reveal a molecular role for AKT/FOXO and JNK/c-JUN in maintaining a differentiation blockade that can be targeted to inhibit leukemias with a range of genetic lesions.

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عنوان ژورنال:
  • Cell

دوره 146  شماره 

صفحات  -

تاریخ انتشار 2011