Abstract
Chemotherapy is a major anticancer therapeutic modality, however, multidrug resistance (MDR) is frequently observed and hinders treatment efficacy. Here, we investigated the role and potential mechanism of the long noncoding RNA (lncRNA) FENDRR in adriamycin resistance of chronic myeloid leukaemia (CML) cells. FENDRR overexpression attenuates adriamycin resistance, as shown by increased Rhodamine 123 accumulation, promotion of cell apoptosis in vitro and suppression of tumour growth in vivo. Mechanistically, we identified that FENDRR reduces the interaction of the RNA-binding protein HuR with MDR1 via acting as a sponge, and miR-184 competitively binds to FENDRR with HuR. Thus, the HuR/FENDRR/miR-184 interaction contributes to MDR1 activity. These findings indicate that FENDRR is a potential target for reversing adriamycin resistance.