Inhibition of autophagy as a treatment strategy for p53 wild-type acute myeloid leukemia.

ABSTRACT: Here we have explored whether inhibition of autophagy can be used as a treatment strategy for acute myeloid leukemia (AML). Steady-state autophagy was measured in leukemic cell lines and primary human CD34⁺ AML cells with a large variability in basal autophagy between AMLs observed. The autophagy flux was higher in AMLs classified as poor risk, which are frequently associated with TP53 mutations (TP53^mut), compared with favorable- and intermediate-risk AMLs. In addition, the higher flux was associated with a higher expression level of several autophagy genes, but was not affected by alterations in p53 expression by knocking down p53 or overexpression of wild-type p53 or p53^R273H. AML CD34⁺ cells were more sensitive to the autophagy inhibitor hydr

SUBMITTER: Folkerts H 

PROVIDER: S-EPMC5550863 | biostudies-literature | 2017 Jul

REPOSITORIES: biostudies-literature