目的探讨Viili多糖对肿瘤特异性抗原基因MAGEA10表达量的影响及其机制。方法利用MTT技术检测不同浓度Viili多糖刺激A549细胞24 h、48 h、72 h后对其存活率的影响,qRT-PCR法检测Viili多糖浓度为10 mg/L、25 mg/L、50 mg/L时与正常生长A549细胞相比较MAGEA10 mRNA相对表达量的变化,并用Western blot检测Viili多糖10 mg/L、25 mg/L、50 mg/L刺激A549细胞后MA-GEA10表达抗原肽的情况。通过MAGEA10 mRNA表达量与抗原肽表达量分析探讨Viili多糖对MAGEA10表达的影响及其表达过程中的可能机制。结果 (1)Viili多糖作用A549细胞后,存活率下降,在0mg/L~50 mg/L范围内其浓度与细胞存活率呈负相关,且作用48 h效果最显著。(2)与未用Viili多糖刺激的空白组相比,Viili多糖浓度为50 mg/L时MAGEA10 mRNA相对表达量上升。(3)与空白组相比,Viili多糖浓度为50 mg/L时MAGEA10蛋白表达量上升。结论 Viili多糖对A549细胞的生长具有一定的抑制作用,上调A549细胞中MAGEA10的转录和翻译水平,两者机制尚需进一步研究,但可能是相互独立的。本研究通过提高癌症的非特异性免疫来提高特异性免疫概率,为癌症辅助治疗提供更多的科学依据。
Objective To discuss the effects and mechanism of MAGEA10 expression in human lung canc- er A549 cells influenced by Viili polysaccharides. Methods MTT was used to study the survival impact of non small cell lung cancer (NSCLC) A549 with viili polysaccharides in different concentration at 24 h, 48 h and 72 h. qRT-PCR was used to detect the relative expression changes of MAGEA10 mRNA with Viili polysaccharides in different concentration of 10 rag/L, 25 mg/L and 50 mg/L compared with those of the normal A549 cells. And Western blot was adopted to detect the antigen expression of MAGEA10 after stimulation of A549 with Villi polysaccharides in different concentration of 10 rag/L, 25 mg/L and 50 mg/L. Through the expression of MAC-EA10 mRNA and antigen, we discussed the effects and possible mechanism of MAGEA10 expression made by Viili polysaccharides. Results (1) Villi polysaccharides inhibited cell proliferation of A549 and its concentration was negatively related to cell survival within 0 mg/L-50 mg/L and the result was most remarkable at 48 h. (2) Compared with the blank group, the relative expression of MAGEA10 mRNA elevated at the concentration of 50 mg/L. (3) Compared with the blank group, the protein expression of MAGEA10 elevated, at the concentration of 50 mg/L. Conclusion Villi inhibited NSCLC A549 cell proliferation, but the increase of the gene transcription and translation levels of MAGEA10 in A549 cell needs further exploration for those two parts might be interdependent. This study aims to indicate that viili is possible to promote non specific immunity, and increase possibility of cancer cell recognition by CTLs, and possibly initiate apoptotic process of cancer cells if same epitope of MAGEA10 and corresponding TCR encounters.