Long noncoding RNAs (lncRNAs) are important regulatory molecules in various biological and pathological processes, including cancer development. We have previously shown that the lncRNA plays an essential role in transforming growth factor-β (TGF-β)-induced epithelial-mesenchymal transition (EMT) of human lung cancer cells. In this study, we investigated the function of another lncRNA, , which shares the locus with , in the regulation of EMT. lncRNA expression was immediately induced during TGF-β-mediated EMT of A549 and LC2/ad lung cancer and Panc1 pancreatic cancer cell lines. overexpression specifically suppressed the expression of and genes, resulting in up-regulation of SNAIL family transcriptional repressor 1 (SNAI1) and SNAI2 transcription factors, which repressed expression of cadherin 1 ()/E-cadherin. Mechanistic investigations revealed that associates with enhancer of zeste 2 polycomb repressive complex 2 subunit (EZH2) protein and induces its recruitment to the regulatory regions of the two microRNA genes for histone H3 methylation and transcriptional repression. Interestingly, expression of both and , but not each individually, could induce EMT-related cell morphological changes and increased cell motility in the absence of TGF-β by activating the gene expression program required for EMT. knockdown indicated that endogenous lncRNA is indispensable for TGF-β-induced EMT in A549 lung cancer and Panc1 pancreatic cancer cells. Our findings indicate that lncRNA significantly contributes to epigenetic EMT induction and increase our understanding of the lncRNA-mediated regulatory mechanisms involved in malignant progression of cancer.