Inhibitory mechanism of curcumin on tumor cells

Abstract

Objective: The aim of this study was to observe the effects of Curcumin (Cur) on the proliferation, invasion, migration and apoptosis of human hepatocellular carcinoma HepG2 cells, and to explore its mechanism of tumor inhibition. Methods: The experimental design encompassed a control group and a CUR group, with HepG2 cells subjected to varying concentrations of CUR solution in vitro culture. Proliferation was assessed using the MTT assay, apoptosis rates, and cell cycle distribution were examined via flow cytometry, and Bcl-2, Bax, and Caspase-3 protein levels were analyzed using Western blot. Migration and invasion capabilities were evaluated using scratch and Transwell assays. Results: A concentration-dependent inhibition of HepG2 cell growth by all CUR concentrations compared to the control group. Flow cytometry demonstrated increased apoptosis rates with rising CUR concentrations, while cell cycle analysis indicated S phase arrest across all groups. Scratch and Transwell assays corroborated a decline in migration and invasion with escalating CUR concentrations. Western blot results illustrated a decrease in Bcl-2 expression and an increase in Bax and Caspase-3 expression compared to the control group. Conclusions: Curcumin emerges as a potent inducer of apoptosis and inhibitor of proliferation in HepG2 cells. Its impact on migration, invasion, and cell division, coupled with the modulation of Bcl-2, Bax, and Caspase-3 proteins, underscores its potential as a therapeutic agent in hepatocellular carcinoma.