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Crocetin induces apoptosis of BGC-823 human gastric cancer cells.

Gastric cancer (GC) is one of the most common types of gastrointestinal tumors worldwide, and the side effects of chemotherapeutic drugs and the resistance to chemotherapy remain problematic in its clinical treatment. Therefore, safe and effective novel agents are urgently required. The purpose of the present study was to investigate the crocetin‑sensitive treatment of GC and its possible mechanisms. BGC‑823 human GC cells were treated with crocetin. The effects of crocetin on the viability of the cells were determined by the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. Hoechst 33258 dyeing and Rh123 staining were used to detect cell apoptosis. The BGC‑823 cells were subjected to western blotting analysis for detection of cytochrome c and cleaved caspase‑3 protein expression. Crocetin inhibited the proliferation of the GC cell line in a dose‑ and time‑dependent manner. Apoptotic BGC‑823 cells induced by crocetin were stained by Hoechst 33258 and observed under a light microscope for cell membrane staining of dense nuclei, nuclear pyknosis, fragmentation, chromatin condensation and highlighted nuclear membrane staining. This revealed a decline in the mitochondrial membrane potential of the BGC‑823 cells. Crocetin also induced caspase‑3 activation and cytochrome c translocation into the cytosol from the mitochondria. The results of this study indicate that crocetin induces the apoptosis of BGC‑823 cells, and may be used as an effective agent in the treatment of GC.