Quercetin induced HepG2 cells apoptosis through ATM/JNK/STAT3 signaling pathways

Liver cancer is the seventh most common malignant tumor in the world and is the second highest cause of death due to cancer. Quercetin, a flavonoid with low toxicity, widely exists in various fruits and vegetables. It has the potential to be a therapeutic agent against various cancers. This study aimed to demonstrate the anti-tumor effect of quercetin on HepG2 cells. Quercetin suppressed the HepG2 cell proliferation in a dose-dependent manner in cell viability assay. Induction of cell apoptosis was confirmed by apoptotic cells population (sub-G1 peak) detected by flow cytometer. A decrease in mitochondrial membrane potential and caspase-3 activation were also demonstrated in this study. Furthermore, quercetin induced HepG2 cell apoptosis through ROS-mediated phosphorylated ataxia-telangiectasia mutated, c-Jun N-terminal kinases, signal transducer, and activator of transcription 3 (STAT-3), and Bax signaling pathways. These results suggest that quercetin has the potential to become an effective drug against the tumor. Superscript/Subscript Available

Automated summary

This study demonstrates the anti-tumor effect of quercetin on HepG2 cells and reveals its mechanism by regulating cell apoptosis and related signaling pathways.