APC基因（家族性结肠腺瘤息肉病）是位于第5号常染色体上，一类大的管家基因，属于肿瘤抑癌基因,编码肿瘤抑制蛋白，作为Wnt信号通路的负向调控因子。该基因的缺陷可导致家族性腺瘤性息肉病，能够发展为恶性肿瘤。肺腺癌组织中的APC基因发生了显著的甲基化改变。本论文以肺腺癌组织DNA为实验样本，对APC基因的第一个外显子启动子区的一段长度为171bp的基因组DNA进行潜在甲基化位点检测。利用甲基化特定PCR方法检测甲基化位点，即首先提取DNA，进行重亚硫酸盐转化修饰，再进行巢式PCR，构建TA克隆载体之后进行菌落PCR，质粒提取和测序。结果：我们已经成功构建了TA克隆载体，以便其甲基化位点测序。而Wn途径调节因子APC表达水平检测结果显示，APC在正常样本的表达水平显著高于肺腺癌样本。因此，在肺腺癌中APC蛋白表达减少上调Wnt途径的信号传导，进而促进肿瘤的发生。

The APC gene (familial adenomatous polyposis) is a large family of household-related genes located on autosomal number 5. It is a tumor suppressor gene and encodes tumor suppressor proteins that act as negative regulators of the Wnt signaling pathway.Defects in the gene can lead to familial adenomatous polyposis, which can develop into malignant tumors. APC gene in lung adenocarcinoma was significantly methylated. In this study, we used lung adenocarcinoma tissue DNA as experimental samples to detect the potential methylation sites of a 171bp genomic DNA in the promoter region of the first exon of APC gene. Methylation specific PCR method was used to detect methylation sites, that is, DNA was extracted first, modified by bisulfite transformation, and then nested PCR was performed to construct TA clone vector, followed by colony PCR, plasmid extraction and sequencing.Results: We have successfully constructed the TA clone vector for the sequencing of its methylation site. The expression level of WN pathway regulator APC in normal samples was significantly higher than that in lung adenocarcinoma samples.Therefore, in lung adenocarcinoma, APC protein expression reduces the signal transduction of the up-regulated Wnt pathway, thereby promoting the occurrence of tumors.