Abstract
Background: microRNAs (miRNAs) have been shown to significantly contribute to the pathogenesis of various tumors, including hepatocellular carcinoma (HCC). Specifically, miR-744-5p has been shown to be associated with tumor development, but the underlying mechanism by which miR-744-5p affects HCC remains unclear. Thus, this study sought to explore the molecular mechanism governing the function of miR-744-5p in HCC. Methods: The expression of miR-744-5p in HCC tissues/cells was detected by quantitative reverse transcription polymerase chain reaction (qRT-PCR). Colony-formation, cell-counting kit 8 (CCK-8), Transwell, and wound-healing assays were used to assess the proliferation and metastasis of HCC cells. Additionally, the interaction between miR-744-5p and transforming growth factor-beta 1 (TGF-β1) was detected using a dual-luciferase reporter and a Western-blot analysis. Results: miR-744-5p expression was shown to be significantly reduced in HCC tissues and cells. The overexpression of miR-744-5p not only significantly inhibited HCC cell proliferation, but also significantly reduced epithelial-mesenchymal transition-induced invasion. A luciferase reporter assay validated the ability of miR-744-5p to directly target TGF-β1. Further, the overexpression of TGF-β1 appeared to abolish the inhibitive effect of miR-744-5p mimics on HCC development. Conclusions: As per our findings, it was revealed that miR-744-5p suppresses HCC proliferation and invasion by regulating the TGF-β1 signaling pathway and epithelial-mesenchymal-transition (EMT).