Circ_0074026 Sponges miR-127-5p to Upregulate RBP7 and Promotes Hepatocellular Carcinoma Progression

Background Circular RNA circ_0074026 has been identified as an oncogenic factor in glioma; however, its expression pattern, biological functions, and underlying mechanisms in hepatocellular carcinoma (HCC) remain largely unexplored. This study aimed to elucidate the regulatory mechanism of the circ_0074026/miR-127-5p/RBP7 axis in HCC progression. Methods The expression levels of circ_0074026, miR-127-5p, and RBP7 were measured in HCC clinical samples and cell lines by RT-qPCR. Pearson correlation analysis was performed to evaluate their interrelationships. Putative binding sites among these molecules were predicted using CircInteractome and CircBank and verified by dual-luciferase reporter and RNA pull-down assays. CCK-8 and colony formation assays were used to assess cell proliferation. Flow cytometry was performed to measure apoptosis. Scratch and Transwell assays were employed to evaluate migration and invasion. Western blotting was conducted to examine the expression of epithelial–mesenchymal transition (EMT)-related proteins. Results Circ_0074026 and RBP7 were significantly upregulated, whereas miR-127-5p was downregulated in HCC tissues and cells. Knockdown of circ_0074026 markedly suppressed HCC cell proliferation, migration, and invasion, promoted apoptosis, and inhibited EMT. Notably, these tumor-suppressive effects were abrogated by either miR-127-5p inhibition or RBP7 overexpression. Mechanistically, circ_0074026 directly sponged miR-127-5p, thereby relieving its repression of RBP7. Conclusions Our findings demonstrate that circ_0074026 drives HCC progression via the miR-127-5p/RBP7 axis, suggesting that this circular RNA represents a potential therapeutic target for HCC patients.