Abstract
Gastric cancer is the fourth most common cause of cancer death globally and the second most common in Asia. Many studies suggest that Crocin has the potential for gastric cancer antineoplastic combined chemotherapy protocols. Here we investigated genomic changes related to the inhibitory effect of Crocin, and elucidated the molecular mechanism of this inhibition in gastric carcinoma cells. We found that, compared with the control group, 216 significantly upregulated and 301 significantly downregulated genes were identified in Crocin-treated AGS cells. Many of these differentially expressed genes in AGS cells are involved in Nrf2-mediated oxidative stress response, p53 signaling, and integrin signaling, which suggested the mechanism of Crocin functions in therapy of gastric cancer. In summary, our study indicates that Crocin has the potential for gastric cancer adjuvant treatment through reducing cell oxidative stress levels.
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