解剖学报
解剖學報
해부학보
ACTA ANATOMICA SINICA
2014年
3期
344-349
,共6页
徐丽%金清东%宫喜%刘卉%周瑞祥
徐麗%金清東%宮喜%劉卉%週瑞祥
서려%금청동%궁희%류훼%주서상
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
褪黑素%小鼠前胃癌細胞%褪黑素膜受體MT2%Akt%ERK1/2%實時定量聚閤酶鏈反應%小鼠
퇴흑소%소서전위암세포%퇴흑소막수체MT2%Akt%ERK1/2%실시정량취합매련반응%소서
Melatonin%Murine foregastic carcinoma cell%Melatonin membrane receptor MT 2%Akt%ERK1/2%Real-time PCR%Mouse
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。
目的:探討褪黑素( MLT)通過褪黑素膜受體MT2抑製小鼠前胃癌( MFC)細胞增殖及其與絲裂原活化蛋白激酶( MAPKs)、燐脂酰肌醇-3激酶( PI3K)-Akt信號通路的關繫。方法應用siRNA技術沉默MT2錶達,觀察褪黑素對小鼠前胃癌細胞的抑製作用及ERK1/2、Akt的燐痠化的影響。結果1.siRNA介導的MT2沉默能明顯拮抗褪黑素對胃癌細胞增殖的抑製作用;2.沉默MT2可部分阻斷褪黑素抑製ERK1/2、Akt燐痠化的作用。結論褪黑素可通過MT2受體抑製ERK1/2、Akt的燐痠化從而抑製胃癌細胞增殖。
목적:탐토퇴흑소( MLT)통과퇴흑소막수체MT2억제소서전위암( MFC)세포증식급기여사렬원활화단백격매( MAPKs)、린지선기순-3격매( PI3K)-Akt신호통로적관계。방법응용siRNA기술침묵MT2표체,관찰퇴흑소대소서전위암세포적억제작용급ERK1/2、Akt적린산화적영향。결과1.siRNA개도적MT2침묵능명현길항퇴흑소대위암세포증식적억제작용;2.침묵MT2가부분조단퇴흑소억제ERK1/2、Akt린산화적작용。결론퇴흑소가통과MT2수체억제ERK1/2、Akt적린산화종이억제위암세포증식。
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 .