| Objective:Gastric cancer is one of the most common malignant diseases in our country and has the very high morbidity and death rate., Notwithstanding the global declining incidence of gastric cancer,it is still one of the most common malignant diseases in our country. DHA is one of the representative materials ofω-3PUFAs. Epidemiological studies have demonstrated a reduced incidence of cancers, including cancers of the breast and colon, and investigators have correlated this with the large quantities ofω-3PUFAs present in their diet. In both animal and cell culture models, this phenomenon was successfully reproduced,indicating thatω-3PUFAs can significantly reduce tumour growth in vivo and suppress cell viability. Nevertheless, despite intense investigation, the precise molecular mechanisms responsible for the anti-tumourigenic properties of co-3PUFAs remain elusive.This study aims to investigate the effects of DHA-induced apoptosis of gastric cancer SGC-7901 cells and the role of ERK1/2 and JNK1/2 MAPK signaling transduction pathway and the apoptosis protein caspase-3.Methods:Gastric cancer SGC-7901 cells was cultured with different concentrations (0,10,30,50μg/mL) of DHA in vitro.The inhibitive effects of DHA on SGC-7901 cells were assessed with MTT assay and apoptosis was evaluated by flow cytometry. The expression of ERK1/2, p-ERK1/2, JNK1/2, P-JNK1/2 and Caspase-3 protein was detected by Western blot.Results:DHA inhibited the proliferation of SGC-7901 cells in a time-and-dose-dependent manner and also induced the apoptosis of SGC-7901 cells. The protein of ERK1/2 was steadily expressed among control and each experimental groups and the protein expression of p-ERK1/2 decreased whereas the activity of caspase-3 increased with the dose of DHA. However, the expression of P-JNK1/2 was not found.Conclusions:DHA may be impact the phosphorylation process of ERK1/2 and regulate the expression of the apoptosis protein caspase-3, which induces apoptosis in gastric cancer cells. |
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