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BACKGROUND Colon cancer (CC) remains a highly malignant cancer, with long non-coding RNAs (lncRNAs) associated with its molecular etiology. OBJECTIVE This study sought to investigate the mechanism of lncRNA prostate cancer-associated transcript 1 (lncRNA PCAT1) in CC cell proliferation and invasion and provide a theoretical reference for CC treatment. METHODS Expression levels of lncRNA PCAT1, microRNA (miR)-128-3p, and SEC61 translocon subunit alpha 1 (SEC61A1) were determined by RT-qPCR. Cell proliferation and invasion were evaluated by cell counting kit-8, colony formation, and Transwell assays. The subcellular fractionation assay analyzed the subcellular localization of lncRNA PCAT1. Dual-luciferase and RNA pull-down assays analyzed the binding of miR-128-3p to lncRNA PCAT1 and SEC61A1. Collaborative experiments were performed with miR-128-3p downregulation or SEC61A1 overexpression in si-PCAT1-treated CC cells. RESULTS LncRNA PCAT1 was upregulated in CC cells, and downregulation of lncRNA PCAT1 reduced CC cell proliferation and invasion potential. LncRNA PCAT1 targeted and inhibited miR-128-3p, and miR-128-3p targeted and inhibited SEC61A1 expression. miR-128-3p inhibition or SEC61A1 overexpression neutralized the suppressive role of silencing lncRNA PCAT1 in CC cell proliferation and invasion. CONCLUSION LncRNA PCAT1 was overexpressed in CC cells and facilitated CC cell proliferation and invasion via inhibition of miR-128-3p and promotion of SEC61A1.