Li Bing-Qiang, Liu Peng-Peng, Zhang Cai-Hua
Department of Gastrointestinal Surgery, Xuzhou Central Hospital, Xuzhou, Jiangsu 221009, P.R. China.
Department of Hepatobiliary Surgery, Xuzhou Central Hospital, Xuzhou, Jiangsu 221009, P.R. China.
Oncol Lett. 2017 Aug;14(2):2315-2319. doi: 10.3892/ol.2017.6455. Epub 2017 Jun 21.
The present study was planned to explore the correlation between the methylation of APC (adenomatous polyposis coli) and colon carcinogenesis. Colon cancer tissues and tumor-adjacent normal tissues of 60 colon cancer patients (who received surgical operation in our hospital from January 2012 to December 2014) were collected. SW1116 cells in human colon cancer tissues were selected for culturing. 5-aza-2c-deoxycytidine (5-aza-dC) was utilized as an inhibitor of the methylation for APC gene. Methylation specific PCR (MSP) was utilized for detection of APC methylation in SW1116 cells. The MTT and Transwell assays were performed to detect the effect of the methylation of APC gene on the proliferation and invasive abilities of SW1116 cells. The correlation between the methylation of APC gene and pathological parameters of colon cancer patients was analyzed. MSP results revealed that 41 cases (68.33%) showed methylation of APC gene in colon cancer tissues. No methylation of APC gene was found in tumor-adjacent normal tissues. 5-aza-dC was able to inhibit the methylation of APC gene in SW1116 cells. APC gene methylation was correlated with tumor size, differentiation degree, lymph node metastasis and Dukes staging. In conclusion, the levels of the methylation of APC in colon cancer tissues and SW1116 cells are relatively high. The methylation of APC promoted the proliferation and invasion abilities of SW1116 cells. Furthermore, methylation is correlated with a variety of clinicopathological features of colon cancer patients.
本研究旨在探讨结肠腺瘤性息肉病(APC)甲基化与结肠癌发生之间的相关性。收集了60例结肠癌患者(2012年1月至2014年12月在我院接受手术治疗)的癌组织及癌旁正常组织。选取人结肠癌组织中的SW1116细胞进行培养。使用5-氮杂-2'-脱氧胞苷(5-aza-dC)作为APC基因甲基化抑制剂。采用甲基化特异性PCR(MSP)检测SW1116细胞中APC的甲基化情况。通过MTT和Transwell实验检测APC基因甲基化对SW1116细胞增殖和侵袭能力的影响。分析APC基因甲基化与结肠癌患者病理参数之间的相关性。MSP结果显示,41例(68.33%)结肠癌组织中存在APC基因甲基化。癌旁正常组织中未发现APC基因甲基化。5-aza-dC能够抑制SW1116细胞中APC基因的甲基化。APC基因甲基化与肿瘤大小、分化程度、淋巴结转移及Dukes分期相关。综上所述,结肠癌组织和SW1116细胞中APC的甲基化水平相对较高。APC甲基化促进了SW1116细胞的增殖和侵袭能力。此外,甲基化与结肠癌患者的多种临床病理特征相关。