Journal of Clinical Hepatology
This article investigates the effects of ectorigenin (TEC) on the proliferation, migration, and apoptosis of hepatocellular carcinoma HepG2 and Huh7 cells, and explores its mechanism of action. The results show that TEC can significantly inhibit cell viability and migration, and promote apoptosis, and its mechanism may be related to the down-regulation of CCNB1 expression, inhibition of MDM2, and activation of the p53 signaling pathway. The study confirmed through the construction of CCNB1 knockdown and overexpression models that the effect of TEC is not significantly enhanced when CCNB1 is lowly expressed, but is antagonized when overexpressed, suggesting that CCNB1 is a key target of TEC. In addition, the combination of HPLC identification and bioinformatics analysis enhances the systematicity of the experiment. The innovation lies in the first revelation that TEC exerts anti-hepatocellular carcinoma effects by regulating the CCNB1-p53 pathway, providing new evidence for the anti-tumor mechanism of natural products. Although the study is limited to in vitro experiments, it lays a foundation for subsequent in vivo verification.
This study systematically explores the antitumor effects and mechanisms of ectorigenin (TEC), a natural isoflavone compound derived from blueberries, on hepatocellular carcinoma cells HepG2 and Huh7. The study found that TEC can significantly inhibit the proliferation and migration of hepatocellular carcinoma cells and promote apoptosis, and its mechanism may be through down-regulating the expression of the cell cycle key protein CCNB1, thereby inhibiting MDM2, stabilizing p53 protein, activating the p53 signaling pathway, and promoting the apoptosis program. Bioinformatics analysis and experimental verification both show that CCNB1 is highly expressed in hepatocellular carcinoma tissues and is associated with poor prognosis, suggesting its potential as a therapeutic target. By constructing CCNB1 knockdown and overexpression models, the study further confirmed that the antitumor effect of TEC depends on the regulation of CCNB1: when CCNB1 is knocked down, TEC has no additional inhibitory effect; while CCNB1 overexpression can resist the effect of TEC, indicating that CCNB1 is a key target for the action of TEC. This study provides solid in vitro experimental evidence for TEC as a potential anti-hepatocellular carcinoma drug, reveals the value of the "CCNB1-p53-MDM2" signaling axis in hepatocellular carcinoma intervention, and is of great significance for the development of low-toxic and effective adjuvant treatment strategies for hepatocellular carcinoma. Subsequent in vivo studies will be conducted to further verify its efficacy.
Objective: To investigate the effect of blueberry-derived tectorigenin (TEC) on hepatocellular carcinoma cell lines HepG2 and Huh7 and …
