Abstract: Objective To investigate the expression and biological function of long non-coding RNA (lncRNA) LINC01614 in colorectal cancer. Methods The expression of LINC01614 in colorectal cancer was analyzed using the TCGA database, and its relationship with patient survival prognosis and clinicopathological features was explored. The function and regulatory pathways involving LINC01614 in colorectal cancer was investigated by Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG), and Gene Set Enrichment Analysis (GSEA). The effect of down-regulated LINC01614 on the proliferation, migration, and invasion of colorectal cancer cells by CCK-8 assay, wound healing assay, and Transwell assay. The relationship between LINC01614 and epithelial-mesenchymal transition (EMT) in colorectal cancer was explored by Western blot and qRT-PCR. Results Compared with adjacent normal tissues, LINC01614 expression was significantly elevated in colorectal cancer tissues (P<0.05), and patients with high LINC01614 expression had significantly lower survival rates than those with low expression (P<0.05). LINC01614 was associated with TNM stage, T stage, and N stage in colorectal cancer patients (P<0.05). LINC01614 may promote cancer progression through the EMT process and the Kirsten rat sarcoma viral oncogene homolog (KRAS) signaling pathway. Downregulation of LINC01614 significantly reduced the proliferation, migration, and invasion of colorectal cancer cells. After downregulating LINC01614 expression, E-cadherin expression was upregulated, while the levels of N-cadherin, Vimentin, and Snail were downregulated. Conclusions LINC01614 is highly expressed in colorectal cancer and associated with patient prognosis and clinicopathological features. LINC01614 promotes the proliferation, migration, and invasion of colorectal cancer cells, potentially by regulating the EMT process through affecting the activity of transcription factor Snail.