LncRNA PVT1 promotes proliferation and migration in gallbladder adenocarcinoma by modulating miR-2355-5p/AGO1 axis.

Abstract

To investigate how lncRNA plasmacytoma variant translocation 1 (PVT1) contributed to the pathogenesis of gallbladder adenocarcinoma (GBA). Bioinformatics techniques were used to analyze differentially expressed lncRNA, and downstream miRNA and mRNA were identified using databases. Quantitative reverse transcription polymerase chain reaction (qRT-PCR) and western blotting were utilized to analyze the RNA and protein expressions in different cells. The binding relationships between different genes were confirmed utilizing luciferase assay and RNA Immunoprecipitation (RIP) assay. Cell growth and migration were examined through CCK-8, colony formation, and Transwell assays. Several in vivo experiments were utilized to determine how the PVT1/miR-2355-5p/AGO1 pathway on tumor growth. Elevated PVT1 was observed in GBA cells, which may further aggravate cell malignant properties. Based on bioinformatics analysis, an interaction between miR-2355-5p and either PVT1 or AGO1 was identified, which was confirmed utilizing dual luciferase reporter assays and RIP assays. Silencing PVT1 (si-PVT1) led to a reduction in AGO1 expression, while depletion of miR-2355-5p reversed this effect. In vivo, PVT1 knockdown significantly inhibited tumor growth, an effect that was reversed by miR-2355-5p downregulation. This study showed that PVT1 facilitated GBA progression via the modulation of the miR-2355-5p/AGO1 axis. These findings underscored the potential therapeutic significance of targeting the lncRNA PVT1 in the treatment of GBA.