Aim. To research the molecular mechanism of ghrelin in apoptosis, migratory, and invasion of gastric cancer (GC) cells. Methods. After GC AGS cells were handled with ghrelin (10^–8 M), cyclooxygenase-2 inhibitor NS398 (100 μM), and Akt inhibitor perifosine (10uM), the rates of apoptosis were detected by TUNEL assay and flow cytometry assay. We assessed the expressions of PI3K, p-Akt, and COX-2 proteins by making use of Western blot analysis. The cell migratory and invasion were detected by using wound-healing and transwell analysis. Results. The migratory and invasion were increased in ghrelin-treated cells, while the rates of apoptosis were decreased. GC AGS cells treated with ghrelin showed an increase in protein expression of p-Akt, PI3K, and COX-2. After cells were treated with Akt inhibitor perifosine, the protein expression of p-Akt, PI3K, and COX-2 and the cell migratory, invasion, and apoptosis were partly recovered. After cells were treated with cyclooxygenase-2 inhibitor NS398, the protein expression of COX-2 and the cell migratory and invasion were decreased, while the rates of apoptosis were increased. Conclusion. Ghrelin regulates cell migration, invasion, and apoptosis in GC cells through targeting PI3K/Akt/COX-2. Ghrelin increases the expression of COX-2 in GC cells by targeting PI3K/Akt. Ghrelin is suggested to be one of the molecular targets in GC.

中文翻译：

---

Ghrelin 调节 Cyclooxygenase-2 表达并促进胃癌细胞进展

瞄准。研究ghrelin在胃癌(GC)细胞凋亡、迁移和侵袭中的分子机制。方法。之后GC AGS细胞用生长素释放肽（10处理^-8  M），环氧合酶-2抑制剂NS398（100  μ M），和Akt抑制剂福辛（10uM的），细胞凋亡的速率通过TUNEL测定检测和流式细胞术检测。我们通过使用蛋白质印迹分析评估了 PI3K、p-Akt 和 COX-2 蛋白的表达。使用伤口愈合和transwell分析检测细胞迁移和侵袭。结果. ghrelin处理的细胞迁移和侵袭增加，而细胞凋亡率降低。用生长素释放肽处理的 GC AGS 细胞显示 p-Akt、PI3K 和 COX-2 的蛋白质表达增加。细胞用Akt抑制剂perifosine处理后，p-Akt、PI3K和COX-2的蛋白表达及细胞迁移、侵袭和凋亡部分恢复。用环氧合酶-2抑制剂NS398处理细胞后，COX-2蛋白表达降低，细胞迁移和侵袭减少，细胞凋亡率增加。结论. Ghrelin 通过靶向 PI3K/Akt/COX-2 调节 GC 细胞中的细胞迁移、侵袭和凋亡。Ghrelin 通过靶向 PI3K/Akt 增加 GC 细胞中 COX-2 的表达。Ghrelin 被认为是 GC 中的分子靶标之一。