The GUSBP11/miR-29c-3p axis facilitates gastric cancer malignancy through ceRNA mechanism

Abstract Background Long non-coding RNAs (lncRNAs) function as pivotal regulators in gastric cancer (GC) pathogenesis via competitive endogenous RNA (ceRNA) networks. However, the precise role of GUSBP11 in GC progression remains inadequately characterized. Aim This investigation aimed to delineate the biological function of GUSBP11 in GC and to ascertain whether it regulates malignant phenotypes via miR-29c-3p. Methods GUSBP11, miR-29c-3p, and THBS2 expression levels were quantified in tissues and cells using RT-qPCR. Prognostic value of GUSBP11 in GC was assessed via Kaplan-Meier curve and Cox analysis. In vitro, AGS and HGC-27 cell lines were employed for loss- and gain-function assays. Cellular viability was measured via CCK-8, while migration and invasion capacities were examined using Transwell chambers. Epithelial-mesenchymal transition (EMT) markers were detected by RT-qPCR. Mechanistic interplay was validated through dual-luciferase reporter assays and miRNA inhibitor rescue experiments. Results GUSBP11 exhibited upregulation in GC tissues and cell lines, correlating significantly with lower 5-year overall survival. Functional assays demonstrated that GUSBP11 overexpression enhanced viability, migration, and invasion, whereas its knockdown elicited the opposite phenotype. Mechanistically, GUSBP11 operated as a ceRNA by sponging miR-29c-3p, thereby relieving suppression of downstream effector THBS2. Co-transfection with a miR-29c-3p inhibitor effectively reversed the tumor-suppressive consequences of GUSBP11 silencing, restoring THBS2 expression and EMT programming. Conclusion The GUSBP11/miR-29c-3p axis exerts a pro-oncogenic influence on GC progression. This regulation offer fresh insights into GC pathophysiology and identifies prospective biomarkers for therapeutic intervention.