中文摘要：

目的本研究的目的是探讨5-氮杂-2’-脱氧胞苷（5-Aza-2’deoxycytidine，5-Aza）对人肺癌细胞系BEl及LTEP-仪-2的增殖和侵袭的调节及其可能的机制。方法两个细胞系均应用5-Aza：进行处理，并应用MTT法检测两细胞系经5-Aza处理后细胞增殖能力的变化，Transwell法检测了两细胞系处理后侵袭能力的变化，Westernblot检测Axin、B—catenin、cyclinD1和MMP-7的表达。结果5-Aza抑制BEl和LTEP-0l-2细胞的增殖和侵袭能力（P〈0．05），与LTEP-a-2细胞系相比，BEl细胞系受抑制程度更为明显（P〈0．05）。5-Aza上调BEl细胞中Axin的表达，抑制B—catenin、cyclinD1和MMP-7的表达，但对LTEP-0l-2细胞中Axin等的表达没有明显的影响。结论5-Aza可以抑制肺癌细胞的增殖和侵袭，BEl细胞中的Axin基因可能存在异常高甲基化，高甲基化的Axin基因可能成为未来治疗肺癌的靶点。

英文摘要：

Objective To explore the effect of 5-aza-2＇-deoxycytidine（5-Aza） treatment on the proliferation and inhibition of human lung cancer cell line BE1 and LTEP- a -2 and their possible mechanism. Methods Two cell lines were treated with 5-Aza, MTr assay was used to test the proliferation of the two cell lines with or without 5-Aza, transwell was used to examine the invasion of the two cell lines with or without 5-Aza. Western blot was used to detect the expression of Axin, 13-catenin, cyclin D1 and MMP-7 in the two cell lines with or without 5-Aza. Results 5-Aza could inhibit the proliferation and invasion of BE1 and LTEP- ct -2 cells （P〈0.05）, compared with LTEP- ct -2 cell line, BE1 cell lines were inhibited more significantly after 5-Aza（p〈0.05）. 5-Aza could upregulate the expression of Axin and inhibit the expressions of 13-catenin, cyclin D1 and MMP-7 in BE1 cells but not in LTEP-ct-2 cells. Conclusion 5-Aza could inhibit the proliferation and invasion of lung cancer cells, abnormal hypermethylated Axin gene might be detected in BE1 cells, hypermethylated Axin gene might become a target for clinical lung cancer treatment.