高级搜索
甲基化修饰对人宫颈癌细胞系中FHIT基因的调控[J]. 肿瘤防治研究, 2007, 34(08): 557-559. DOI: 10.3971/j.issn.1000-8578.181
引用本文: 甲基化修饰对人宫颈癌细胞系中FHIT基因的调控[J]. 肿瘤防治研究, 2007, 34(08): 557-559. DOI: 10.3971/j.issn.1000-8578.181
Pattern of FHIT Gene 5'CpG Island Methylation Contribute to Human Cervical Carcinoma Cell Tumorigenesis[J]. Cancer Research on Prevention and Treatment, 2007, 34(08): 557-559. DOI: 10.3971/j.issn.1000-8578.181
Citation: Pattern of FHIT Gene 5'CpG Island Methylation Contribute to Human Cervical Carcinoma Cell Tumorigenesis[J]. Cancer Research on Prevention and Treatment, 2007, 34(08): 557-559. DOI: 10.3971/j.issn.1000-8578.181

甲基化修饰对人宫颈癌细胞系中FHIT基因的调控

Pattern of FHIT Gene 5'CpG Island Methylation Contribute to Human Cervical Carcinoma Cell Tumorigenesis

  • 摘要: 目的 探讨FHIT在子宫颈癌发生中的作用及FHIT基因失活的机制。方法 培养宫颈癌细胞C-33A、HeLa、CasKi、SiHa及人脐静脉血管内皮细胞ECV-304,进行5-aza-dC干预前后FHIT基因在5株细胞中的甲基化分析,并通过逆转录聚合酶链式反应和免疫荧光化学染色方法检测5-aza-dC干预前后FHIT基因在5株细胞中的表达。结果 4种宫颈癌细胞均存在FHIT基因的甲基化,正常对照细胞ECV-304在5-aza-dC干预前后均未见明显FHIT基因扩增产物。4株宫颈癌细胞在5-aza-dC化学干预前均未见明显FHIT的荧光着色,而干预后的细胞胞浆中可见FHIT的表达强度明显增强,尤其在10-6 M及2×10-6 M干预浓度下的表达最强(P〈0.05);干预48h、72h后FHIT的表达与干预24h的类似。ECV-304细胞在5-aza-dC化学干预前后的胞浆均可见到FHIT的阳性表达,其表达强度之间无明显差异(P〉0.05)。结论 FHIT基因的甲基化在宫颈癌中是频发事件,甲基化可能是FHIT基因沉默及宫颈癌发生的重要机制。

     

    Abstract: Objective  To determine whether hypermethylation of FHIT played an important role in cervical tumorigenesis. Methods  By incubating DNA in the presence of a methylase, we investigated the methylation of FHIT in four cervical cancer cell lines and one human umbilical vein endothelial cell line treating with the DNA methyltransferase inhibitor, 5-aza-2'-deoxycytidine (5-aza-dC) . The expression of FHIT was also monitored by RT-PCR and immunofluorescence technique before and af ter 5-aza-dC treatment . Results  We found that methylation of FHIT occured in the four cervical cancer cell lines instead of the ECV-304. Through RT-PCR and immunofluorescence technique, we found that the expression of FHIT, which could hardly be detected in all four cervical cancer cells, was significant different af ter 5-aza-dC treatment . However, the ECV-304 cell expressed FHIT at constant levels before and af ter 5-aza-dC t reatment . Conclusion  We concluded that hypermethylation of FHIT gene occurred f requently in cervical tumorigenesis. And hypermethylation within the regulatory sequences of FHIT gene might be an important means for its inactivation in cervical cancer.

     

/

返回文章
返回