Abstract
BACKGROUND: Propofol is an anesthetic used in clinical surgery. Many studies have shown that propofol has the potential to kill cancer cells; however, the mechanism by which it kills hepatocellular carcinoma (HCC) cells remains unclear. METHODS: To examine this issue, the apoptosis change of HepG2 and Huh-7 cell lines treated with propofol were observed. Additionally, a quantitative reverse-transcriptase polymerase chain reaction was used to measure the expression level of hsa-miR-134 (miR-134), and a Cell Counting Kit-8 assay and flow cytometry assay were used to observe cell apoptosis. A dual-luciferase assay was used to confirm the binding effect of miR-134 and BCL-2 (B cell lymphoma-2), and a western blot assay was used to detect expression level changes of BCL-2 and cleaved caspase-3. RESULTS: The results showed that propofol significantly promoted HepG2 and Huh-7 cell apoptosis, and that miR-134 expression level is related to the concentration of propofol. The dual-luciferase assay showed that miR-134 significantly reduced the luciferase activity of BCL-2-wt, but had no notable effect on BCL-2-mut. In rescue experiments, miR-134 deficiency resulted in a high apoptosis rate, a low BCL-2 expression level, and a high cleaved caspase-3 expression level induced by propofol in HepG2. CONCLUSIONS: In summary, propofol appears to upregulate the expression level of miR-134, decrease the BCL-2 level, and induce HCC cell apoptosis by promoting the cleaved caspase-3 expression level. TRIAL REGISTRATION: Chinese Clinical Trial Registry ChiCTR18000199.