A549肺癌细胞株中癌睾丸抗原的表达及生物学意义研究

Cancer Testis Antigen Expression and Regulation of A549 and Biological Meaning

目的:癌睾丸抗原(cancer-testis antigen,CTA)是一类主要表达于睾丸组织和癌组织,并具有较强诱导体液和细胞免疫应答能力的抗原,可以作为抗肿瘤的理想靶分子。本研究探讨了A549肺癌细胞系中CTA的表达情况及其生物学意义。方法:本研究中选取了A549肺癌细胞株,运用RT-PCR的方法检测了其中九种常见CTA的表达情况,进一步通过AV-PI双染法观察了表柔比星,紫杉醇,卡铂,伊立替康,依托泊苷五种化疗药物对A549细胞的凋亡作用及其调控CTA表达的情况。另外用转化生长因子β1(TGF-β1)处理A549细胞,验证了TGF-β1促进细胞生长的作用,进一步检测此时CTA的表达调控。结果:结果显示MAGEA1,MAGEA3,MAGEC1,HCA661在A549细胞系中稳定表达,表柔比星能够强烈诱导细胞发生凋亡,其诱导作用岁浓度增高而增强。表柔比星下调了MAGEA1,MAGEA3,MAGEC1的表达,对HCA661的表达无影响。TGF-β1增强了肿瘤细胞增殖能力,与此同时下调HCA661的表达,对MAGEA1,MAGEA3,MAGEC1的表达无影响。结论:MAGEA1,MAGEA3,MAGEC1,HCA661在肺癌细胞系A549中稳定表达。TGF-β1作用48小时,使HCA661的表达下调,MAGEA1,MAGEA3,MAGEC1的表达无变化。表柔比星作用48小时,使MAGEA1,MAGEA3,MAGEC1的表达下调,HCA661表达无影响,卡铂,紫杉醇,伊立替康,依托泊苷对CTA的表达无调控,为进一步明确CTA的表达调控机制奠定了研究基础,同时为将HCA661作为临床中诊断与治疗的新靶点提供了可行性。

Objective： Cancer-testis antigens （CTA）are a series of antigens which mostly expressed in testis and cancer cells, and have strong capacity of inducing humoral and cellular immunity. They are promising as vaccine to tumor. In this investigation, we detect the expression and regulation of CT antigens in A549 cell line. Methods： Nine kinds of CT antigens are detected of their expression in A549 cell line using the method of RT-PCR. Also the role of TGF-β1 and five kinds of chemotherapy medicine playing in the regulation of CT antigens is investigated. Results： The results show that MAGEA1, MAGEA3, MAGEC1, HCA661 express in A549 cell line. TGFβ1 down-regulates the expression ofHCA661, but has no effect on MAGEA1, MAGEA3 and MAGEC1. Epirubicin down-regulates the expression of MAGEA1, MAGEA3 and MAGEC1, but have no effect on HCA661. Conclusion： MAGEA1, MAGEA3, MAGEC1, HCA661 stably express in A549 lung cancer cell line. For 48 hours, TGF-β1 down-regulate the expression of HCA661, MAGEA1, MAGEA3, MAGEC1, unchanged. Epirubicin down-regulate the expression of MAGEA1, MAGEA3 and MAGEC1, but it does not affect HCA661. Carboplatin, paclitaxel, irinotecan, etoposide have no CT antigen expression regulation. Our study laid the basis for further clarification of the mechanism of CTA expression regulation and provided feasibility of HCA661 as a new target for clinical diagnosis and treatment.