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目的:探讨去甲基化药物5-杂氮-2-脱氧胞苷(5-aza-2-deoxycytidine,5-aza-CdR)对鼻咽癌5-8F细胞Syk基因启动子去甲基化作用及其侵袭转移的影响。方法:利用5-aza-CdR处理体外培养的5-8F细胞,采用BS-PCR、Q-RT-PCR、Western Blot及Transwell方法分别检测药物干预前后5-8F细胞中Syk甲基化、Syk mRNA、Syk蛋白及穿膜细胞数的情况。结果:经5-aza-CdR处理后5-8F细胞株的甲基化水平降低(P<0.01),Syk mRNA及蛋白表达升高(P<0.05),其侵袭及转移能力降低(P<0.05),且呈剂量依赖性。结论:鼻咽癌细胞Syk基因启动子甲基化导致其基因沉默,Syk基因失表达,从而引起鼻咽癌细胞的侵袭转移能力增加,5-aza-CdR可以使鼻咽癌细胞Syk基因启动子去甲基化,使因甲基化沉默的Syk基因重新表达,恢复其抑制肿瘤细胞侵袭转移的能力。
AIM: To investigate the demethylation of Syk gene promoter in nasopharyngeal carcinoma 5-8F cells by 5-aza-2-deoxycytidine (5-aza-CdR) And the impact of invasion and metastasis. Methods: 5-8F cells cultured in vitro were treated with 5-aza-CdR. Syk methylation, Syk mRNA expression in 5-8F cells were detected by reverse transcription-polymerase chain reaction (RT-PCR), Western blot and Transwell assay respectively. , Syk protein and the number of transmembrane cells. Results: The methylation level of 5-8F cells decreased (P <0.01) and the expression of Syk mRNA and protein increased (P <0.05), while the invasion and metastasis ability of 5-8F cells decreased (P <0.05 ), And in a dose-dependent manner. CONCLUSIONS: Syk gene promoter methylation in nasopharyngeal carcinoma cells leads to silencing of Syk gene and loss of expression of Syk gene, leading to increased invasion and metastasis of nasopharyngeal carcinoma cells. 5-aza-CdR can induce Syk gene promoter Demethylation, re-expression of Syk gene due to methylation silencing, restoring its ability to inhibit the invasion and metastasis of tumor cells.