Recently, much evidence shows that long noncoding RNAs (IncRNAs) significant role in human tumorigenesis.By using publicly available expression profiling data in lung cancer and integrating bioinformatics analyses, we screened out a H3K27-acetylation-activated LINC01116, whose expression is significantly increased and is correlated with outcomes in non-small cell lung cancer (NSCLC).Further experiments found that LINC01116 could regulate proliferation of NSCLC both in vitro and in vivo.RNA-seq analysis revealed that LINC01116 knockdown preferentially affected genes that are linked to antitumor immune responses and inflammation-related genes.Mechanistic investigations found that LINC01116 serves as a scaffold for two distinct epigenetic modification complexes (5domain of LINC01116 binding Polycomb Repressive Complex 2 (PRC2) while 3domain of LINC01116 binding DNMT1) and modulates the transcription of IRF7 (interferon regulatory factor 7) and CD 1D (CD1D molecule) in nucleus.And knockdown of LINC01116 promoted the activation and cytotoxicity of NKT cells via epigenetic-mediated upregulating CD1D expression on NSCLC cells.In cytoplasm, LINC01116 regulates Survivin as a molecular decoy for miR-145-5p, a microRNA that targets both LINC01116 and Survivin, thus facilitating cell survival.Together, we have identified the LINC01116-mediated immune inhibition of which restricts immunosurveillance to enable malignant growth of NSCLC and promote formation of a cancer immune evasion phenotype.Our data demonstrated the important roles of LINC01116 in NSCLC oncogenesis and might serve as targets for NSCLC diagnosis and therapy.