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BACKGROUND PD-L1 enhanced the tumorigenesis and immune escape abilities of cancers. The upstream mechanisms of PD-L1 in regulating tumorigenesis and immune escape of diffuse large B cell lymphoma (DLBCL) remained unclear. METHODS Human DLBCL cell line OCI-Ly10 and DLBCL patient samples were used in this study. MALAT1 was knocked down by shRNA. MiR-195 was inhibited by miR-195 inhibitor. Levels of MALAT1, PD-L1, miR-195 and CD8 were detected by RT-qPCR. Protein levels of PD-L1, Ras, p-ERK1/2, ERK1/2, Slug, E-cadherin, N-cadherin, Vimentin were detected by western blotting. The interaction between MALAT1 and miR-195, miR-195 and PD-L1 were detected by luciferase assay. OCI-Ly10 cell proliferation and apoptosis were detected by MTT and Annexin V/PI assays, respectively. Migration was detected by transwell assay. Cytotoxicity of CD8+ T cells was detected by LDH cytotoxicity kit. Proliferation and apoptosis of CD8+ T cell co-cultured with OCI-Ly10 cells were analyzed by CFSE and Annexin V/PI staining. RESULTS MALAT1, PD-L1 and CD8 were up-regulated in DLBCL tissues while miR-195 was down-regulated. MiR-195 was negatively correlated with MALAT1 and PD-L1. MALAT1 could sponge miR-195 to regulate the expression of PD-L1. MALAT1 increased miR-195 level and decreased PD-L1 level. It also inhibited cell proliferation, migration and immune escape ability while increased apoptosis ratio of OCI-Ly10 cells. shMALAT1 treatment in OCI-Ly10 cells also promoted proliferation and inhibited apoptosis of CD8+ T cells. Knocking down of MALAT1 also suppressed EMT process via Ras/ERK signaling pathway. These effects were all rescued by miR-195 inhibitor. CONCLUSION Long non-coding RNA MALAT1 sponged miR-195 to regulate proliferation, apoptosis and migration and immune escape abilities of DLBCL by regulation of PD-L1.