Long non-coding RNAs (lncRNAs) have been shown to play important regulatory roles in the pathogenesis and progression of multiple cancers. Here, we investigated the role of long intergenic non coding RNA 319 (linc00319) in the proliferation and invasion of lung cancer cells. We found that, compared with normal lung cell line HBE, linc00319 was increased in low metastatic lung cancer cell lines PAa and AgiY-83a, and further increased in high metastatic lung cancer cell lines A549 and Anip-973. Then, different concentrations of pcDNA-linc00319 expression vector and different concentrations of linc00319 siRNA were respectively transfected into A549 lung cancer cells. The results showed that linc00319 increased the proliferation and invasion of A549 cells, and suppressed cell apoptosis, in a dose-dependent manner. In contrast, linc00319 siRNA suppressed A549 cell proliferation and invasion, and promoted cell apoptosis, in a dose-dependent manner. The online bioinformatic tool RNAhybrid revealed that linc00319 potentially bound with the miR-32, which functioned as a tumor suppressor in lung cancer. Luciferase acitivity and RNA pull-down assays comfirmed that linc00319 directly bound with miR-32. Linc00319 could negatively regulate the expression of miR-32 and positively regulate the protein levels of miR-32 target genes, including AURKA, SOX9 and TWIST1. In conclusion, linc00319 promotes cell proliferation and invasion in lung cancer cells by directly binding with and downregulating the tumor suppressor miR-32.