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首页> 外文期刊>Oncology letters >DNA hypermethylation of the vimentin gene inversely correlates with vimentin expression in intestinal- and diffuse-type gastric cancer
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DNA hypermethylation of the vimentin gene inversely correlates with vimentin expression in intestinal- and diffuse-type gastric cancer

机译：在肠道和弥漫型胃癌中，波形蛋白基因的DNA高甲基化与波形蛋白表达呈负相关

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摘要

The vimentin gene is a hallmark of epithelial-to-mesenchymal transition and has been observed to be overexpressed in various types of tumor cell line and tissue. Previous studies have reported correlations between vimentin DNA methylation levels and subsequent vimentin expression levels in solid tumors, including breast and colorectal cancer; however, to the best of our knowledge, such a correlation has not been reported for gastric cancer (GC) using Lauren classification. Therefore, the present study aimed to quantify DNA methylation levels of the vimentin gene using quantitative (q) methylation-specific polymerase chain reaction (PCR) in intestinal-type GC cell lines (MKN-28, AGS and MKN-1), diffuse-type GC cell lines (SGC-7901, SNU-5 and KATO III), the GES-1 immortalized human non-neoplastic gastric epithelial cell line, as well as in tumor and paratumor normal tissue samples. Furthermore, the present study analyzed the messenger RNA expression of the vimentin gene in these cell lines and tissues by reverse transcription-qPCR. A comparison of the clinicopathological features was conducted between patients, grouped according to the Lauren classification. The present study identified that the vimentin promoter region was hypermethylated in all GC cell lines and tumor tissue samples when compared with immortalized normal gastric epithelial cells and paratumor normal tissues. In addition, vimentin promoter methylation levels were observed to be higher in intestinal-type cell lines when compared with those of diffuse-type lines and tissues. Correspondingly, vimentin expression levels were lower in intestinal-type gastric cell lines compared with those of diffuse-type cell lines and tissues, and were lowest in the non-neoplastic gastric cell line and paratumor normal tissues. Patients with diffuse-type GC were on average younger (P=0.023), and exhibited higher tumor (P=0.020), node (P=0.032) and TNM classification of malignant tumor stage (P=0.039) than those with intestinal-type GC. Following treatment of AGS cells (which demonstrated the highest methylation level of the vimentin gene) with 5-aza-2'-deoxycytidine, vimentin expression was restored significantly. Thus, the present study revealed that vimentin promoter methylation levels are inversely correlated with vimentin expression levels in GC (according to Lauren classification). High levels of methylation in the vimentin gene promoter region may be involved in carcinogenesis and the development of GC, and may provide a novel molecular classification for GC.
机译：波形蛋白基因是上皮到间充质转化的标志，并且已观察到在各种类型的肿瘤细胞系和组织中过表达。先前的研究已报道波形蛋白DNA甲基化水平与随后波形蛋白表达水平在包括乳腺癌和结肠直肠癌在内的实体瘤中的相关性。然而，据我们所知，尚未使用Lauren分类法报道胃癌（GC）的这种相关性。因此，本研究旨在通过定量（q）甲基化特异性聚合酶链反应（PCR）在肠型GC细胞系（MKN-28，AGS和MKN-1），弥漫性肝细胞癌中量化波形蛋白基因的DNA甲基化水平。类型的GC细胞系（SGC-7901，SNU-5和KATO III），GES-1永生化的人非肿瘤性胃上皮细胞系，以及肿瘤和癌旁正常组织样品。此外，本研究通过逆转录-qPCR分析了波形蛋白基因在这些细胞系和组织中的信使RNA表达。根据Lauren分类对患者之间的临床病理特征进行了比较。本研究发现，与永生化的正常胃上皮细胞和癌旁正常组织相比，波形蛋白启动子区域在所有GC细胞系和肿瘤组织样品中均甲基化。另外，与分散型细胞系和组织相比，在肠型细胞系中波形蛋白启动子甲基化水平更高。相应地，与分散型细胞系和组织相比，肠型胃细胞系中波形蛋白的表达水平较低，在非肿瘤性胃细胞系和癌旁正常组织中波形蛋白的表达水平最低。弥漫型GC患者平均较小肠类型的患者年轻（P = 0.023），并且表现出更高的肿瘤（P = 0.020），淋巴结转移（P = 0.032）和恶性肿瘤分期的TNM分类（P = 0.039）。 GC。用5-氮杂-2'-脱氧胞苷处理AGS细胞（证明波形蛋白基因的甲基化水平最高）后，波形蛋白的表达显着恢复。因此，本研究显示波形蛋白启动子甲基化水平与GC中波形蛋白表达水平成反比（根据Lauren分类）。波形蛋白基因启动子区域中的高水平甲基化可能与癌变和GC的发展有关，并可能为GC提供新的分子分类。

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