聚肌胞苷酸对肺癌细胞A549生长和功能影响

Effect of polycytidine monophasphate on the growth and function of lung adenocarcinoma A549

探讨聚肌胞苷酸(polyI∶C)对肺腺癌细胞(A549)增殖、周期、凋亡及γδT细胞对其杀伤活性的影响。用MTT法检测经polyI∶C处理后的γδT细胞和A549的生长抑制率;流式细胞仪检测经polyI∶C处理后A549 TLR3变化及对细胞周期和凋亡的影响;用乳酸脱氢酶释放法测定γδT细胞对经polyI∶C诱导后的A549杀伤活性。肺癌细胞株A549经25μmol/L polyI∶C诱导24 h后细胞凋亡率为(39.44%±4.11%),明显高于对照组凋亡率(28.72%±1.41%)(P<0.05);细胞周期有一定的改变;肿瘤细胞上TLR3表达没有明显变化。A549在25μmol/L PolyI∶C处理后,其与γδT细胞在效靶比为1∶80时杀伤活性明显高于对照组。polyI∶C能抑制A549细胞生长,增加γδT细胞对诱导后的A549细胞杀伤敏感性。

The effect of polycytidine monophosphate（polyI∶C） on the proliferation,cycle,apoptosis and the influence of gamma delta T cells（γδT） on its killer activity were investigated in the present study.By using MTT method,the growth inhibition rate of γδT cells and A549 cells after treatment with polyI∶C were measured.Flow cytometric analysis was used to detect the influence of poly I∶C in the changes to express TLR3,cell cycle and apoptosis of A549 cells.Meanwhile,LDH analysis was used to test the killing activity of γδT cells to cancer cells after induction with polyI∶C.It was demonstrated that the apoptotic rate of the lung adenocarcinoma A549 cells after induction with polyI∶C（25 mol/L） was 39.44 ＋ 4.11%,which was significantly higher than that of the controls（28.7 ＋1.41%）,（P0.05）.Under this condition,the cell circle had some changes,but the expression of TLR4 on cancer cells showed no change.The killing activity of γδT cells to A549 cells in a effector-target radio of 1∶8 was also significantly higher than that of the controls.It is evident that polyI∶C can inhibit the growth of the lung adenocarcinoma A549 cells and can increase the killing sensitivity of these cells to the action of γδT cells after induction with polyI∶C.