%0 Journal Article
%T Che-1 is targeted by c-Myc to sustain proliferation in pre-B-cell acute lymphoblastic leukemia.
%A Folgiero V
%A Sorino C
%A Pallocca M
%A De Nicola F
%A Goeman F
%A Bertaina V
%A Strocchio L
%A Romania P
%A Pitisci A
%A Iezzi S
%A Catena V
%A Bruno T
%A Strimpakos G
%A Passananti C
%A Mattei E
%A Blandino G
%A Locatelli F
%A Fanciulli M
%J EMBO Rep
%V 19
%N 3
%D 03 2018
%M 29367285
%F 9.071
%R 10.15252/embr.201744871
%X Despite progress in treating B-cell precursor acute lymphoblastic leukemia (BCP-ALL), disease recurrence remains the main cause of treatment failure. New strategies to improve therapeutic outcomes are needed, particularly in high-risk relapsed patients. Che-1/AATF (Che-1) is an RNA polymerase II-binding protein involved in proliferation and tumor survival, but its role in hematological malignancies has not been clarified. Here, we show that Che-1 is overexpressed in pediatric BCP-ALL during disease onset and at relapse, and that its depletion inhibits the proliferation of BCP-ALL cells. Furthermore, we report that c-Myc regulates Che-1 expression by direct binding to its promoter and describe a strict correlation between Che-1 expression and c-Myc expression. RNA-seq analyses upon Che-1 or c-Myc depletion reveal a strong overlap of the respective controlled pathways. Genomewide ChIP-seq experiments suggest that Che-1 acts as a downstream effector of c-Myc. These results identify the pivotal role of Che-1 in the control of BCP-ALL proliferation and present the protein as a possible therapeutic target in children with relapsed BCP-ALL.