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MT2受体介导褪黑素对小鼠胃癌细胞的抑制作用
Inhibitory effect of melatonin on murine foregastric carcinoma cells via membrane receptors MT2
目的 探讨褪黑素（MLT）通过褪黑素膜受体MT2抑制小鼠前胃癌（MFC）细胞增殖及其与丝裂原活化蛋白激酶（MAPKs）、磷脂酰肌醇-3激酶（PI3K)-Akt信号通路的关系。方法 应用siRNA技术沉默MT2表达，观察褪黑素对小鼠前胃癌细胞的抑制作用及ERK1/2、Akt的磷酸化的影响。结果 1.siRNA介导的MT2沉默能明显拮抗褪黑素对胃癌细胞增殖的抑制作用；2. 沉默MT2可部分阻断褪黑素抑制ERK1/2、Akt磷酸化的作用。结论 褪黑素可通过MT2受体抑制ERK1/2、Akt的磷酸化从而抑制胃癌细胞增殖。
Objective To investigate the inhibitory effect of melatonin on the proliferation activity of murine foregastic carcinomac (MFC) cells via melatonin membrane receptors MT2 and its relationship with the signaling pathways of mitogen-activated protein kinases (MAPKs), phosphatidylinositol 3-kinase(PI3K)-Akt. Methods Using siRNA technology to silence MT2 expression, we examined the ability of melatonin to inhibit the proliferation activity of MFC cells and its influence on the phosphorylation of ERK1/2 and Akt. Results We found two interesting effects of SiRNA-mediated silencing of MT2 expression. Firstly, it significantly antagonized the inhibitory effect of melatonin on the proliferation activity of MFC cells. Secondly, it partially blocked the inhibitory effect of melatonin on the phosphorylation of ERK1/2 and Akt. Conclusion Our results suggest that melatonin can inhibit the phosphorylation of ERK1/2 and Akt via MT2 receptors, thereby inhibiting the proliferation of gastric cancer cells.
褪黑素 / 小鼠前胃癌细胞 / 褪黑素膜受体MT2 / Akt / ERK1/2 / 实时定量聚合酶链反应 / 小鼠
Melatonin / Murine foregastic carcinoma cell / Melatonin membrane receptor MT2 / Akt / ERK1/2 / Real-time PCR / Mouse
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