摘要
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 MT 2 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 ERK 1/2 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 ERK 1/2 and Akt.Conclusion Our results suggest that melatonin can inhibit the phosphorylation of ERK 1/2 and Akt via MT2 receptors , thereby inhibiting the proliferation of gastric cancer cells .
出处
《解剖学报》
CAS
CSCD
北大核心
2014年第3期344-349,共6页
Acta Anatomica Sinica
基金
国家自然科学基金资助项目(30971541)
福建省科技厅重点资助项目(2012Y0033)
福建省自然科学基金资助项目(2012J01411)
莆田市科技计划资助项[2012S11(2)]