Objective: To investigate the effects and mechanism of long non-coding RNA colon cancer-associated transcript-1 (ncCRNA CCAT1) on the proliferation and metastasis of lung cancer cells by regulating miR-181a-5p. Methods: The expression of CCAT1 and miR-181a-5p in lung cancer cell lines A549, PC-9 and H226 and normal human bronchial epithelial cells 16HBE were detected by qRT-PCR. The bioinformatics software and dual luciferase reporter gene were used to detect the targeted regulation of CCAT1 and miR-181a-5p. The lung cancer cell line with the highest CCAT1 expression was routinely cultured, which was divided into NC group, si-CCAT1 group and si-CCAT1+miR-181a-5p inhibitor, cells were transfected with blank, CCAT1 siRNA and CCAT1 siRNA+miR-181a-5p inhibitor, respectively. The expression levels of CCAT1 and miR-181a-5p in each group were detected by qRT-PCR. The effects of CCAT1 on the proliferation of cells in each group were detected by MTS and plate cloning. The effect of CCAT1 on the cell metastasis ability of each group was detected by Transwell. The activity of the MAPK signaling pathway in the cells of the group was detected by Western blotting. Results: Compared with 16HBE in normal human bronchial epithelial cells, the expression of CCAT1 was increased in lung cancer cell lines, and the expression of miR-181a-5p was decreased in lung cancer cell lines. CCAT1 has the highest expression in A549 cells. Compared with the NC group, CCAT1 was down-regulated in the si-CCAT1 and si-CCAT1+miR-181a-5p inhibitor groups; compared with the si-CCAT1 group, CCAT1 was increased in the si-CCAT1+miR-181a-5p inhibitor group. compared to the NC group, miR-181a-5p was increased in the si-CCAT1 and si-CCAT1+miR-181a-5p inhibitor groups; compared to the si-CCAT1 group, miR-181a-5p expression was reduced in the si-CCAT1+miR-181a-5p inhibitor group. Bioinformatics software and dual luciferase reporter gene results showed that CCAT1 has a binding site with miR-181a-5p. Compared with the NC group, the proliferation, metastasis and MAPK signaling pathways of the si-CCAT1 and si-CCAT1+miR-181a-5p inhibitor groups were decreased; compared with the si-CCAT1 group, the cell proliferation, metastasis ability and MAPK signaling pathway activity of si-CCAT1+miR-181a-5p inhibitor group were increased. Conclusion: CCAT1 promotes the proliferation and metastasis of lung cancer cells by regulating miR-181a-5p. CCAT1 may be a potential target for the treatment of lung cancer.