摘要
目的 探讨肿瘤细胞 p16基因CpG岛过甲基化对其表达的影响。 方法 利用甲基化特异性PCR (MSP)检测了 4种肿瘤细胞 (SPC A1、BIU 87、T2 4、HepG2 )的甲基化状态 ,并通过RT PCR检测该 4种肿瘤细胞在用去甲基化试剂 5 氮杂脱氧胞苷 (5 Aza CdR)处理前后表达程度的差异。结果 除BIU 87外 ,其它 3种肿瘤细胞p16基因都有不同程度的甲基化 ,用 5 Aza CdR处理后比处理前 p16mRNA的表达有显著升高。 结论 p16基因CpG岛的过甲基化可导致转录表达失活 ,与肿瘤的发生、发展关系密切。
Objective To study the status of methylation of p16 gene CpG island and the impact to its transcriptional inactivation due to hypermethylation in several tumor derived cell lines. Methods The status of methylation in 4 tumor derived cell lines (SPC A1, BIU 87, T24, HepG2) was detected by means of methylation specific polymerase chain reaction (MSP) and the difference in the expression of p16 by using RT PCR before and after treatment with 5 aza 2′ deoxycytidine (5 Aza CdR). Results With the exception of BIU 87, the remaining tumor derived cell lines had methylation to verying degrees. The expression of p16 mRNA after treatment of the cells with 5 Aza CdR was significantly increased as compared with that before treatment.Conclusion The promoter methylation of p16 CpG island can result in its transcriptional inactivation, which may be close related to the development of tumor.
出处
《华中科技大学学报（医学版）》
CAS
CSCD
北大核心
2004年第2期132-135,共4页
Acta Medicinae Universitatis Scientiae et Technologiae Huazhong
基金
国家自然科学基金资助项目 (No .39990 5 70 )
