CAJ | 학술논문

目的探讨瘦素促进肺腺癌A549细胞增殖的分子机制.方法瘦素处理A549细胞,Western blotting方法检测细胞内Bcl-2的表达；MAPK及PI3K信号通路阻滞剂处理A549细胞,Western blotting方法检测信号通路下游复合物ERK1/2、p-ERK1/2、Akt、p-Akt等蛋白及细胞内Bcl-2的表达变化.结果瘦素促进细胞内Bcl-2的表达,且具有浓度依赖性.瘦素可促进ERK1/2、Akt的磷酸化；用MAPK及PI3K信号通路阻滞剂预处理细胞,可以阻滞ERK1/2、Akt的磷酸化,并能够抑制Bcl-2蛋白的表达.结论瘦素可能通过MAPK和PI3K通路,介导抗凋亡蛋白Bcl-2的过度表达而使肺腺癌A549细胞呈持续增殖,从而为开发抗肿瘤药物提供新思路.
목적 탐토수소촉진폐선암A549세포증식적분자궤제.방법 수소처리A549세포,Western blotting방법검측세포내Bcl-2적표체；MAPK급PI3K신호통로조체제처리A549세포,Western blotting방법검측신호통로하유복합물ERK1/2、p-ERK1/2、Akt、p-Akt등단백급세포내Bcl-2적표체변화.결과 수소촉진세포내Bcl-2적표체,차구유농도의뢰성.수소가촉진ERK1/2、Akt적린산화；용MAPK급PI3K신호통로조체제예처리세포,가이조체ERK1/2、Akt적린산화,병능구억제Bcl-2단백적표체.결론 수소가능통과MAPK화PI3K통로,개도항조망단백Bcl-2적과도표체이사폐선암A549세포정지속증식,종이위개발항종류약물제공신사로.
Objective To investigate the possible molecular mechanism of leptin in stimulating the proliferation of lung adenocarcinoma A549 cells.Methods A549 cells were treated with different concentrations of leptin,and the expression of Bcl-2 was evaluated by Western blotting.The expressions of ERK1/2,p ERK1/2,Akt,p-Akt,and Bcl-2 were detected by Western blotting after MAPK and PI3K signaling pathway blockers were used.Results Leptin increased the expression of Bcl-2 in a dosedependent manner.Leptin also caused ERK1/2 and Akt phosphorylation.Pretreatment with inhibitors of MAPK and PI3K inhibited these responses,and abolished Bcl-2 expression.Conclusions Leptin may mediate the over-expression of anti-apoptotic gene Bcl-2 by activating MAPK and PI3K pathway to promote the continues proliferation of A549 cells,and may represent a target for anticancer drug development.