SOX2-Induced Linc-ROR Upregulation Inhibits Gastric Carcinoma Cell Proliferation and Metastasis Via the miR-580-3p/ANXA10 Pathway.

Abstract

Previous studies have proven that long intergenic non-coding RNA regulator of reprogramming (Linc-ROR) plays opposing roles in different cancer types. This work intended to investigate its functions and underlying mechanisms in gastric carcinoma (GCa) progression. RT-qPCR was utilized for gene expression measurement. GCa cell viability, apoptosis, migration, and invasion were detected by functional assays, including CCK-8, flow cytometry, and Transwell assays. ChIP assay and Dual-luciferase reporter assay were utilized to affirm the associations between genes. Linc-ROR expression dramatically declined in GCa tissues and cell lines. Linc-ROR upregulation suppressed GCa cell proliferation, migration, and invasion but accelerated GCa cell apoptosis. As for Linc-ROR-associated molecular mechanisms in GCa, SOX2 associated with Linc-ROR promoter region to activate Linc-ROR transcription in GCa cells; Linc-ROR upregulated ANXA10 level in GCa cells by competitively binding to miR-580-3p. As revealed by rescue assays, Linc-ROR-induced inhibition on malignant biological behaviors of GCa cells could be partially abated by ANXA10 deletion or miR-580-3p upregulation. SOX2-activated Linc-ROR serves as a cancer suppressor to restrain GCa progression in vitro via the miR-580-3p/ANXA10 pathway, suggesting a promising diagnostic and therapeutic target for GCa patients.