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目的 观察亚砷酸钠 (NaAsO2 )和砷酸钠 (Na3 AsO4 )对人支气管上皮BEP2D细胞p16基因甲基化及表达的影响。方法 采用甲基化特异性PCR(MSP)及RT PCR等技术观察分析BEP2D细胞p16基因甲基化和表达水平。结果 (1)NaAsO2 (0 0 16～ 2 μmol/L)和高浓度组Na3 AsO4 (80和16 0 μmol/L) 具有促进BEP2D细胞p16基因二核苷酸CpG岛甲基化作用 ;而低浓度组Na3 AsO4 (2 0和40 μmol/L) 不能使BEP2D细胞p16基因CpG岛发生甲基化。 (2 )无机砷可使BEP2D细胞p16基因表达下降 ,且NaAsO2 较Na3 AsO4 更为明显。结论 无机砷可引起BEP2D细胞p16基因CpG岛甲基化程度增高和表达水平下降 ,提示p16基因高甲基化是无机砷致癌的可能途径之一。
Objective To investigate the effects of sodium arsenite (NaAsO2) and sodium arsenite (Na3 AsO4) on the methylation and expression of p16 gene in human bronchial epithelial cells (BEP2D). Methods Methylation-specific PCR (MSP) and RT-PCR techniques were used to analyze the methylation and expression of p16 gene in BEP2D cells. Results (1) NaAsO2 (0 0 16 ~ 2 μmol / L) and high concentrations of Na3 AsO4 (80 and 160 μmol / L) could promote methylation of dinucleotide CpG island of p16 gene in BEP2D cells. Group Na3 AsO4 (20 and 40 μmol / L) did not methylate p16 CpG island in BEP2D cells. (2) Inorganic arsenic decreased the expression of p16 gene in BEP2D cells, and NaAsO2 was more obvious than Na3AsO4. Conclusion Inorganic arsenic can cause the methylation of CpG island of p16 gene in BEP2D cells to decrease and its expression level decrease, suggesting that hypermethylation of p16 gene is one of the possible pathways of inorganic arsenic carcinogenesis.