Objective To investigate the effect of long non-coding RNA (lncRNA) -MIAT on autophagy in diffuse large B-cell lymphoma (DLBCL) cells by regulating micRNA (miR) -584/ ZESTE homolog enhancer 2 (EZH2) axis. Methods DLBCL cell line Raji was divided into a silenced group for lncRNA-MIAT using small interfering RNA (siMIAT group), a silenced negative control group (siNC group), a mimic group for miR-584 (mimic group), and a mimic negative control group (mimic-NC group). The siMIAT group of Raji was further divided into an inhibitor group for miR-584 (inhibitor group), an inhibitor negative control group (inhibitor-NC group), an EZH2 overexpression group (pcDNA-EZH2 group), and an overexpression empty vector group (pcDNA-null group). Real-time quantitative PCR (qRT-PCR) was used to detect the expression of lncRNA-MIAT and miR-584, while fluorescence in situ hybridization (FISH) experiment was used to detect the localization of lncRNA-MIAT in Raji. Western blot was used to detect the expression of EZH2 and autophagy markers LC3-I, LC3-II, Atg5, Beclin-1, and p62. CCK-8 assay was used to detect cell proliferation activity. Dual luciferase reporter gene analysis was used to analyze the targeted regulation of miR-584 and EZH2, as well as the targeted regulation of miR-584 and lncRNA-MIAT. Results The results showed that compared with normal human B lymphocyte cell line MAO, lncRNA-MIAT was highly expressed in Raji (P＜0.05) and was mainly located in the cytoplasm. Silencing lncRNA-MIAT inhibited cell proliferation activity and autophagy (both P＜0.05), while also inhibiting EZH2 expression and promoting miR-584 expression (both P＜0.05). Bioinformatics analysis predicted that lncRNA-MIAT and miR-584 had multiple binding sites, as well as EZH2 and miR-584. Dual luciferase reporter gene experiments confirmed that EZH2 was a target gene of miR-584, and that lncRNA-MIAT also had a targeted regulatory effect on miR-584. In cells with silenced lncRNA-MIAT, cell proliferation activity and autophagy increased in the inhibitor group compared with the inhibitor negative control group (both P＜0.05). In cells with silenced lncRNA-MIAT, cell proliferation activity and autophagy increased in the pcDNA-EZH2 group compared with the pcDNA-null group (both P＜0.05).Conclusion lncRNA-MIAT promotes autophagy in lymphoma cells by targeting the miR-584/EZH2 axis