MIR9-3HG/let-7c-5p/THBS1 axis promotes hepatocellular carcinoma progression

Background Long non-coding RNAs (lncRNA) are key regulators in hepatocellular carcinoma (HCC). However, the role of MIR9-3HG in HCC remained unclear. Objective This study investigated the expression, clinical significance, and molecular mechanism of MIR9-3HG in HCC. Methods MIR9-3HG, hsa-let-7c-5p, and THBS1 levels were quantified via RT-qPCR in 179 paired HCC tissues and cell lines. Associations between MIR9-3HG expression and clinicopathological features were analyzed using χ 2 test. The prognostic value was assessed using Kaplan-Meier and Cox regression analyses. The biological functions of MIR9-3HG were evaluated through CCK-8, Transwell assays. The competing endogenous RNA (ceRNA) targeting relationship was validated using dual-luciferase reporter. Results MIR9-3HG was significantly upregulated in HCC tissues and cell lines. High MIR9-3HG expression correlated with advanced TNM stage, higher Edmondson-Steiner grade, vascular invasion, and poor overall survival, and was identified as an independent prognostic factor. Hsa-let-7c-5p expression was negatively correlated with MIR9-3HG and THBS1in HCC tissues. In vitro experiments, silencing MIR9-3HG inhibited HCC cell proliferation, migration, and invasion. Luciferase reporter assays demonstrated that MIR9-3HG functioned as a ceRNA to sponge hsa-let-7c-5p. In turn, hsa-let-7c-5p directly targeted and negatively regulated THBS1. Conclusion MIR9-3HG promoted HCC aggressiveness by acting as a ceRNA for hsa-let-7c-5p to upregulate THBS1. These findings highlighted its potential as a prognostic biomarker.