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Overexpression of LncRNA-HOTAIR promotes chemoresistance in acute leukemia cells.

Chemotherapy treatment of acute myeloid leukemia (AML) can be compromised due to the multidrug resistance (MDR) of leukemia cells. HOTAIR, a long noncoding RNA (LncRNA), is involved in MDR development of various solid tumors. However, whether it functions in MDR development of leukemia remains unclear. In this study, expressions of HOTAIR in leukemia cell line K562/A02 and bone marrow samples from 10 patients with refractory and relapsed AML were detected by qRT-PCR. The apoptosis, proliferation, and susceptibility of K562/A02 cells to Adriamycin (ADR) were analyzed by flow cytometry and CCK8 assay, respectively. The expression of cell cycle regulator P21 and Notch1 in the K562/A02 cells was examined by qRT-PCR. The accumulation of total AKT and the phosphorylated AKT (pAKTS473) were detected by western blotting. We found that the expression of HOTAIR in drug-resistant cells and patient samples was increased. Inhibition of HOTAIR expression could suppress the proliferation, increase the apoptosis, and promote the doxorubicin sensitivity of K562/A02 cells. Moreover, inhibiting expression of HOTAIR could attenuate the expression of P21 and Notch1 and inhibit the phosphorylation of AKT in drug-resistant cells. In conclusion, our results demonstrated that LncRNA-HOTAIR is involved in MDR development of leukemia cells by regulating the expression of P21 and the AKT/Notch1 signaling pathway.