Epigenetically regulated expression of ALDH1 by anthracyclines causes an adaptive oxidative response and drug resistance in AML
To investigate drug-induced epigenetic resistance in AML, the K562 cell line was selected due to its responsiveness to anthracyclines and its ease of genetic manipulation. Daunorubicin (DNR) was chosen as a model drug because of its pivotal role in AML treatment. DNR treatment of K562 cells induced expression of all three ALDH1 isoforms. To explore the activation of cis-regulatory elements, ChIP-Seq with H3K27Ac was performed on K562 cells treated or not with DNR for 18 hours. Overall design: In vitro and in vivo validation of daunorubicin-induced enhancers associated to drug resistance in Acute Myeloid Leukemia.