血管生成素-2对人结肠癌细胞SW1116增殖的影响及其机制

目的探讨血管生成素-2(Angiopoietin-2,Ang-2)对人结肠癌细胞SW1116增殖的影响及其机制。方法用不同浓度的Ang-2处理SW1116细胞,MTT法检测其对SW1116细胞增殖的影响;将SW1116细胞分为正常对照、无血清DMEM、Ang-2(1.2 mg/L)及PI3K/Akt阻断剂LY294002(10μmol/L)+Ang-2组,作用24 h后,MTT法检测LY294002对SW1116细胞增殖的影响,Western blot分析Tie-2、PI3K和Akt蛋白的表达。结果 Ang-2在1.2 mg/L时,对SW1116细胞增殖的影响最显著;LY294002能有效抑制由Ang-2引起的SW1116细胞的增殖;Ang-2组与无血清DMEM组比较,Tie-2的表达略有上升,但差异无统计学意义(P>0.05),Akt蛋白的表达显著增强(P<0.01),而PI3K蛋白的表达显著降低(P<0.01),LY294002+Ang-2组中3种蛋白的表达与Ang-2组相比,均明显降低(P均<0.01)。结论 Ang-2能促进SW1116细胞增殖,LY294002可抑制由Ang-2引起的SW1116细胞的增殖,其机制可能与Tie-2/PI3′-kinase/Akt调节的信号通路有关。

Effect of Angiopoietin-2 on Proliferation of Human Colon Cancer SW1116 Cells and Relevant Mechanism

Objective To investigate the effect of angiopoietin-2(Ang-2) on proliferation of human colon cancer SW1116 cells as well as the relevant mechanism.Methods SW1116 cells were treated with Ang-2 at various concentrations and determined for proliferation level by MTT method.The cells were divided into normal control,serum-free DMEM,Ang-2(1.2 mg / L) and PI3K / Akt inhibitor LY294002(10 μmol / L) + Ang-2 groups,then determined for proliferation level by MTT method,and for expressions of Tie-2,PI3K and Akt proteins by Western blot 24 h after treatment.Results Compared with that at other concentrations,1.2 mg / L Ang-2 influenced the proliferation of SW1116 cells significantly.LY294002 inhibited the proliferation of SW1116 cells caused by Ang-2 effectively.Compared with those in serum-free DMEM group,the expression level of Tie-2 increased slightly(P > 0.05),and that of Akt increased significantly(P < 0.01),while that of PI3K decreased significantly(P < 0.01).However,all the expression levels of the proteins were significantly lower in LY294002 + Ang-2 group than in Ang-2 group(P < 0.01).Conclusion Ang-2 promoted the proliferation of SW1116 cells,which can be inhibited by LY294002 by a possible mechanism associated with the signal pathway regulated by Tie-2 / PI3′-kinase / Akt.