Conclusion
The present study highlighted the possibility of using Mag as a novel therapeutic drug for HCC treatment.
Methods
The HepG2 cells were treated with varying concentrations of Mag (10, 20, and 30 μM) for 48 hours. The effects of Mag on the proliferation, migration, invasion, apoptosis and cell cycle progression of HepG2 cells were respectively detected by MTT assay, transwell assays, and flow cytometric analysis. A HepG2 cell-based tumor-bearing model was established to evaluate the effect of Mag on HCC tumor growth in vivo. The protein expression levels were determined by Western blot analysis.
Results
Our results showed that Mag inhibited the proliferation, migration, and invasion of HepG2 cells in vitro in a dose-dependent manner. In addition, Mag reduced the HCC tumor volume and weight in the mouse xenograft model. Subsequent studies showed that Mag induced apoptosis in HepG2 cells, accompanied by a loss in mitochondrial membrane potential, cytochrome c release, and induction of endoplasmic reticulum stress. Furthermore, inhibition of the endoplasmic reticulum stress by CHOP knockdown restored the effects of Mag in HepG2 cells.