BACKGROUND The purpose of the present study was to investigate the role of the methylation status of the DACT1 gene on the invasion and metastasis of nasopharyngeal carcinoma cells. METHODS The levels of methylation and expression of the DACT1 gene in nasopharyngeal carcinoma tissues and CNE2 cells were determined by methylation-specific PCR and RT-PCR, respectively. CNE2 cells were treated with 5-aza-2-deoxycytidine, and the variation in the methylation status of the DACT1 gene was detected, as well as the influence of methylation on invasiveness of nasopharyngeal carcinoma cells. RESULTS The DACT1 gene was hyper-methylated in 44 of 62 cases of nasopharyngeal carcinoma. The DACT1 gene was hyper-methylated in 32 of 38 cases of nasopharyngeal carcinoma with lymph node metastasis, and the DACT1 gene was hyper-methylated in 7 of 24 cases of nasopharyngeal carcinoma without lymph node metastasis. The DACT1 mRNA level was weakly expressed or not expressed in all nasopharyngeal carcinoma tissues with hyper-methylated DACT1 genes; however, the DACT1 mRNA level was highly expressed in nasopharyngeal carcinoma tissues with low expression of the methylated DACT1 gene. The DACT1 gene was hyper-methylated and not expressed in CNE2 cells that did not have 5-aza-2-deoxycytidine treatment. After 5-aza-2-deoxycytidine treatment, the DACT1 gene was demethylated and the expression of DACT1 was restored. Moreover, the invasion ability was inhibited in CNE2 cells treated with 5-aza-2-deoxycytidine. CONCLUSION The expression of DACT1 was related to the methylation status. High expression of DACT1 may inhibit the invasion and metastasis of nasopharyngeal carcinoma cells.

中文翻译：

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DACT1甲基化状态对鼻咽癌侵袭和转移的影响。

背景技术本研究的目的是研究DACT1基因的甲基化状态在鼻咽癌细胞的侵袭和转移中的作用。方法采用甲基化特异性PCR和RT-PCR分别检测鼻咽癌组织和CNE2细胞的甲基化水平和DACT1基因的表达。用5-氮杂-2-脱氧胞苷处理CNE2细胞，检测DACT1基因的甲基化状态的变化，以及甲基化对鼻咽癌细胞侵袭性的影响。结果62例鼻咽癌中有44例DACT1基因被甲基化。在38例具有淋巴结转移的鼻咽癌中，有32例中DACT1基因被高度甲基化，在24例无淋巴结转移的鼻咽癌中，有7例DACT1基因被高度甲基化。在所有具有高甲基化DACT1基因的鼻咽癌组织中，DACT1 mRNA的表达均弱表达或不表达。然而，DACT1 mRNA水平在鼻咽癌组织中高表达，而甲基化DACT1基因却低表达。DACT1基因被高度甲基化，未在未进行5-氮杂-2-脱氧胞苷处理的CNE2细胞中表达。在5-氮杂-2-脱氧胞苷处理后，DACT1基因被去甲基化并恢复了DACT1的表达。此外，在用5-氮杂-2-脱氧胞苷处理的CNE2细胞中，侵袭能力受到抑制。结论DACT1的表达与甲基化状态有关。