Isobavachalcone induces the apoptosis of gastric cancer cells via inhibition of the Akt and Erk pathways

In the present study, the MGC803 gastric cancer cell line was used as an experimental model to evaluate the potential role of isobavachalcone (IBC) in cell apoptosis, migration and invasion. The inhibitory effects of IBC on cell proliferation were determined using a methylthiazolyltetrazolium assay. Cellular morphological changes were assessed using Wright-Giemsa staining, and cell apoptosis was evaluated by flow cytometric analysis. The results of the present study demonstrated that IBC inhibited the proliferation of MGC803 cells in a concentration- and time-dependent manner. Furthermore, the wound healing and Matrigel™ Transwell® invasion assays demonstrated that IBC decreased cell migration and invasion in a concentration-dependent manner. Western blotting was used to determine the protein expression levels of caspase-3, B-cell lymphoma-2 (Bcl-2) and Bcl-2-associated X protein (Bax), as well as the key protein kinases in the Akt and extracellular signal-regulated kinase (Erk) signaling pathways. During the IBC-induced apoptosis of MGC803 cells, transient activation of phosphorylated (p)-Akt and p-Erk inhibited the activation of Akt and Erk, upregulated Bax expression, downregulated Bcl-2 expression and activated caspase-3. These results suggest that IBC inhibited the growth of MGC803 gastric cancer cells by regulating the protein expression of caspase-3, Bcl-2 and Bax. In addition, inhibition of the Akt and Erk signaling pathways may be important mechanisms underlying the IBC-induced apoptosis of gastric cancer cells.