RESUMEN
PURPOSE: Gastric cancer causes high mortality rates across the globe, mainly due to late diagnosis and the unavailability of effective chemotherapeutic agents. This study evaluated the anticancer potential of plumbagin against gastric cancer cells as well as its effects on autophagic and apoptotic pathways, cell migration and invasion. METHODS: MTT assay was used for cell viability assessment. Acridine orange (AO)/ethidium bromide (EB) and annexin V/propidium iodide (PI) staining were used for the detection of apoptosis. Autophagy was demonstrated by electron microscopy. Transwell assay was used for cell migration and invasion. Western blotting was used for the detection of protein expression. RESULTS: The results showed that plumbagin could considerably inhibit the proliferation of AGS gastric cancer cells (IC50;8 µM). The anticancer activity of plumbagin against AGS cells was found to be due to the induction of autophagy and apoptosis. Plumbagin-induced apoptosis and autophagy were also associated with alteration in apoptosis (Bax and Bcl-2) and autophagy (LC3I, II, and Beclin 1) - related protein expressions. The effects of plumbagin on the migration and invasion of AGS cells were also investigated by transwell assays and the results showed that plumbagin inhibited both the migration and invasion of AGS cells at IC50. CONCLUSIONS: These results indicate that plumbagin significantly inhibits the growth of gastric cancer in vitro and could prove beneficial in the management of gastric cancer and needs further research including in vivo studies.