LncRNA CTB-31O20.2 promotes the progression of hepatocellular carcinoma by targeting the miR-139-5p/ROCK1 axis

Abstract

Hepatocellular carcinoma (HCC) is a primary cause of mortality from cancer, necessitating novel insights into its molecular underpinnings. Recent evidence points to the significant roles of lncRNAs in HCC progression, among which CTB-31O20.2 has emerged as a potentially crucial player. This study utilized RNA sequencing to identify differentially expressed lncRNAs in HCC tissues, focusing on CTB-31O20.2. We employed RT-qPCR, Western blotting, and dual-luciferase reporter assays to evaluate the expression patterns of CTB-31O20.2 in HCC cells and its interactions with miR-139-5p and Rho-associated coiled-coil containing protein kinase1 (ROCK1). In vivo effects were analyzed using a xenograft mouse model. CTB-31O20.2 was significantly upregulated in HCC tissues and cell lines. Silencing CTB-31O20.2 in Hep3B and HepG2 cells reduced malignancy, evidenced by decreased viability, colony formation, and invasion, and increased apoptosis. These cellular behaviors were associated with alterations in apoptosis-related proteins and epithelial-mesenchymal transition (EMT) markers. CTB-31O20.2 was shown to interact with miR-139-5p, and its silencing upregulated miR-139-5p, leading to reduced ROCK1 expression. Conversely, miR-139-5p inhibition reversed the anti-tumor effects of CTB-31O20.2 silencing. Overexpression of ROCK1 negated the inhibitory effects on HCC cell malignancy induced by CTB-31O20.2 depletion. In vivo, CTB-31O20.2 silencing significantly reduced tumor growth in a xenograft model. Our findings reveal that CTB-31O20.2 contributes to HCC progression by modulating miR-139-5p and ROCK1 expression. These results highlight CTB-31O20.2 as a potential therapeutic target in HCC, providing a new perspective on the mechanisms driving HCC pathogenesis and progression.