The Cerna Network of Long Non-Coding RNA PCAT1/Mir-128-3p/SEC61A1 In Colon Cancer Cell Proliferation and Invasion.

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.