LncRNA LINC00265/miR-485-5p/IRF2-mediated autophagy suppresses apoptosis in acute myeloid leukemia cells.

Background: Extensive studies have shown that long non-coding RNAs (lncRNAs) play important roles in multiple cancers. The present study aimed to investigate the role and mechanism of lncRNA LINC00265 in the regulation of apoptosis in acute myeloid leukemia (AML) cells. Methods: Gain- or loss-of-function experiments were conducted in AML cells to explore the effect of LINC00265 on AML. Autophagy was assessed by examining levels of Beclin-1, p62, and ratio of LC3-II/LC3-I. Cell proliferation and apoptosis of AML cells were evaluated by CCK-8 assay and flow cytometry, respectively. RNA pull-down was performed to enrich miR-485-5p interacted with LINC00265. The interaction between miR-485-5p and IRF2 3'UTR was analyzed by luciferase reporter assay. Results: LINC00265 expression was significantly up-regulated, whereas miR-485-5p was down-regulated in serum of AML patients and AML cell lines. LINC00265 promoted, whereas miR-485-5p suppressed autophagy in AML cells. Mechanistically, LINC00265 functioned as a ceRNA for miR-485-5p to facilitate IRF2 expression. More importantly, LINC00265 overexpression or miR-485-5p inhibitor reversed the 3-methyladenine (3-MA, an autophagy inhibitor)-mediated proliferation-inhibitory and pro-apoptotic effects, whereas LINC00265 silencing or miR-485-5p mimic overturned the proliferation-promoting and anti-apoptotic effects of autophagy activator rapamycin. Conclusion: LINC00265 attenuates AML cell apoptosis by inducing autophagy via miR-485/IRF2 axis.