异丙酚下调PKM2抑制人肺腺癌细胞系增殖、迁移和侵袭

目的探讨异丙酚对肺腺癌细胞增殖、迁移和侵袭的影响。方法 MTT法检测异丙酚(60、100、120μmol/L)处理的人肺腺癌细胞系A549、Anip973的抑制率或增殖;将si-NC组(转染si-NC)、si-PKM2(丙酮酸激酶M2)组(转染si-PKM2)、pc DNA3. 1组(转染pc DNA3. 1)、pc DNA3. 1-PKM2组(转染pc DNA3. 1-PKM2)用脂质体法转染至Anip973细胞,部分组用120μmol/L异丙酚处理;Transwell小室法检测细胞迁移和侵袭;RT-qPCR检测细胞中PKM2的mRNA的表达;Western blot检测细胞中PKM2、E-cadherin、MMP-2的蛋白表达。结果异丙酚(60、100和120μmol/L)呈浓度依赖性抑制人肺腺癌细胞A549、Anip973增殖(P <0. 05),Anip973细胞对异丙酚的敏感性较强,最适浓度为120μmol/L;异丙酚可抑制Anip973细胞迁移和侵袭,并下调PKM2、MMP-2蛋白表达,上调E-cadherin蛋白表达;敲减PKM2具有与异丙酚相同的抑制Anip973细胞的增殖、迁移和侵袭作用,下调MMP-2蛋白表达,上调E-cadherin蛋白表达的作用;过表达PKM2可减轻异丙酚对Anip973细胞增殖、迁移和侵袭及E-cadherin、MMP-2蛋白表达。结论异丙酚可抑制肺腺癌细胞系的增殖、迁移和侵袭,其机制与下调PKM2表达相关。

Propofol inhibits proliferation,migration and invasion of human lung adenocarcinoma cell lines through down-regulating PKM2

Objective To investigate the mechanism of propofol on proliferation,migration and invasion of lung adenocarcinoma cells. Methods MTT method was used to detect the inhibition rate or proliferation of A549 and Anip973 human lung adenocarcinoma cell lines treated with propofol( 60,100,120 μmol/L);The si-NC group( transfected si-NC),the si-PKM2 group( transfected si-PKM2),pcDNA3. 1 group( transfected pcDNA3. 1),pcDNA3. 1-PKM2 group( transfected pcDNA3. 1-PKM2),propofol + pcDNA3. 1 group( transfected pcDNA3. 1 and treated with propofol),propofol + pcDNA3. 1-PKM2 group( transfected pcDNA3. 1-PKM2 and treated with propofol),all were transfected into Anip973 cells by liposome and treated with propofol;Transwell assay was used to detect cell migration and invasion;RT-qPCR was used to detect the expression of PKM2 mRNA in cells;Western blot was used to detect protein expression of PKM2,E-cadherin,MMP-2,in cells. Results Propofol( 0,60,100,120 μmol/L) inhibited the proliferation of human lung adenocarcinoma cells A549 and Anip973 in a concentration-dependent manner. Anip973 cells were more sensitive to propofol,and the optimal concentration was120 μmol/L;propofol inhibited the proliferation,migration and invasion of Anip973 cells,down-regulated the protein expression of PKM2 and MMP-2,and up-regulated the protein expression of E-cadherin;knockdown of PKM2 has the same inhibition effect as propofol proliferation,migration and invasion,down-regulate the protein expression of MMP-2 and up-regulate the protein expression of E-cadherin of Anip973 cells;over-expression of PKM2 reversed the proliferation,migration and invasion,the effect of protein expression of E-cadherin and MMP-2 of Anip973 cells. Conclusions Propofol inhibits the proliferation,migration and invasion of lung adenocarcinoma cells,and its mechanism is related to down-regulation of PKM2 expression.