Journal of Clinical Hepatology
This article investigates the effects of gallic acid (GA) on the proliferation, migration, invasion, and apoptosis of human liver cancer HepG2 cells, as well as its molecular mechanism. The results show that GA can significantly inhibit the activity of HepG2 cells, with an IC50 of (18.36±1.54) μg/mL after 48 hours, and it inhibits cell proliferation, migration, and invasion ability in a time and dose-dependent manner. Flow cytometry shows that after 48 hours of GA treatment, the apoptosis rate of cells significantly increases and is dose-dependent (13.27%, 20.94%, 40.74% in the 5–20 μg/mL groups, respectively), with a significant difference compared to the control group. Western Blot results indicate that GA downregulates the expression of MMP-2, MMP-9, and anti-apoptotic protein Bcl-2, while upregulating the expression of pro-apoptotic protein Bax and Cleaved caspase-3, suggesting that it induces apoptosis by regulating the mitochondrial apoptosis pathway. The innovation lies in systematically revealing that GA exerts its anticancer effect by regulating the Bax/Bcl-2/Caspase-3 signaling axis and inhibiting MMPs expression, providing experimental evidence and theoretical support for the use of the natural product GA as a potential antitumor drug.
This study explores the effects of gallic acid (GA) on the proliferation, migration, invasion, and apoptosis of human liver cancer HepG2 cells and its mechanism of action, which has important theoretical and potential application value. Firstly, GA significantly inhibits the proliferation ability of HepG2 cells, showing that with increasing concentration, the number of cell colonies is significantly reduced, and it is dose-dependent, indicating its strong antitumor proliferation effect. Secondly, GA can significantly reduce the migration and invasion ability of HepG2 cells, as shown by the Transwell experiment, where the number of cells passing through the membrane decreases after treatment with different concentrations of GA, indicating that it may act by inhibiting the potential of tumor cell metastasis. In addition, flow cytometry results show that GA can induce apoptosis, and Western blot further reveals that it may achieve the above effects by regulating the expression of MMP-2, MMP-9, and apoptosis-related proteins. These findings provide experimental evidence for GA as a potential anticancer drug, expands the research ideas of natural compounds in the field of tumor treatment, and has certain transformation prospects. At the same time, the study is designed in accordance with norms, including multi-method verification, which enhances the reliability of the results.
Objective: To investigate the effect of gallic acid (GA) on the proliferation, migration, invasion, and apoptosis of human hepatocell…
