| 刘学智,南晶,李娟,李颖,丁玲,王金桃.FHIT基因甲基化及蛋白表达与HPV16感染在宫颈癌变中的交互效应[J].中华流行病学杂志,2016,37(6):858-862 |
| FHIT基因甲基化及蛋白表达与HPV16感染在宫颈癌变中的交互效应 |
| Interaction between fragile histidine triad methylation, protein expression and human papillomavirus 16 infection in cervical carcinogenesis |
| 收稿日期:2016-01-13 出版日期:2016-06-14 |
| DOI：10.3760/cma.j.issn.0254-6450.2016.06.023 |
| 中文关键词: 宫颈癌变 人乳头瘤病毒16型 FHIT基因 交互效应 |
| 英文关键词: Cervical carcinogenesis Human papillomavirus 16 Fragile histidine triad gene Interaction |
| 基金项目:国家自然科学基金(30872166,81273157,81473060);山西省自然科学基金(2008011075-1) |
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| 中文摘要: |
| 目的 探讨脆性组氨酸三联体(FHIT)基因甲基化及蛋白表达异常与HPV16感染在宫颈癌变中的作用及其交互效应。方法 选择2009年9月至2011年3月在山西省肿瘤医院、山西医科大学第二医院妇科、太原市妇幼保健院和介休市妇幼保健院就诊的宫颈鳞状细胞癌(SCC)新发患者100例,宫颈上皮内瘤样变(CIN)患者142例(72例CIN1,70例CIN2+)和正常宫颈(NC)妇女108例为研究对象。采用多重PCR法检测HPV16感染状况,应用甲基化特异性PCR(MSP)和Western Blot法分别检测FHIT基因甲基化状态和蛋白的表达水平。利用SPSS 20.0软件进行相关资料的t检验、方差分析、χ2检验、因素与疾病关联效应分析(OR值及其95%CI),应用相加效应模型进行交互作用评价。结果 HPV16感染率在CIN1组(45.8%)、CIN2+组(68.6%)和SCC组(73.0%)均高于NC组(28.7%),差异均有统计学意义(P<0.001);在NC、CIN1、CIN2+和SCC组,FHIT基因甲基化率分别为3.7%、13.9%、21.4%和38.0%,蛋白表达水平分别为1.255±0.130、1.184±0.172、1.133±0.126和1.099±0.148,各组的差异均有统计学意义(P<0.001);随宫颈病变程度的加重,HPV16感染率逐渐升高(趋势检验χ2=47.623,P<0.001),FHIT基因甲基化率逐渐升高(趋势检验χ2=40.147,P<0.001),FHIT蛋白低表达率也逐渐升高(趋势检验χ2=65.098,P<0.001);FHIT基因高甲基化、FHIT蛋白低表达与HPV16感染在不同宫颈病变组均存在正相加交互效应。结论 FHIT基因高甲基化和FHIT蛋白低表达与HPV16感染均可增加宫颈癌及其癌前病变的发生风险,FHIT基因高甲基化和FHIT蛋白低表达与HPV16感染在宫颈癌变中均具有协同作用。 |
| 英文摘要: |
| Objective To investigate the association between fragile histidine triad (FHIT) gene methylation, abnormal protein expression and HPV16 infection as well as their interactions in cervical carcinogenesis. Methods A total of 108 patients with normal cervical (NC), 142 cases of cervical intraepithelial neoplasia (CIN1, n=72; CIN2+, n=70), and 100 new cases of cervical squamous cell carcinoma (SCC) were chosen from the Shanxi Tumor Hospital, Second Hospital of Shanxi Medical University, Maternal and Child Health Center in Taiyuan and Jiexiu during September 2009 and March 2011. HPV16 was detected by multiple PCR. FHIT methylation and protein expression levels were detected by methylation specific PCR (MSP) and Western Blot, respectively. All the data were performed with SPSS 20.0 statistical software. Differences among groups were assessed by Chi-square and Kruskal-Wallis tests. The interaction effects were evaluated by additive model. Results The prevalence rates of HPV16 infection in CIN1 (45.8%), CIN2+ (68.6%) and SCC (73.0%) were significantly higher than that in NC (28.7%, P<0.001). In NC, CIN1, CIN2+ and SCC groups, the FHIT gene methylation rates were 3.7%, 13.9%, 21.4% and 38.0% while the protein expression levels were 1.255±0.130, 1.184±0.172, 1.133±0.126 and 1.099±0.148, respectively. Differences among the groups were statistical significant (P<0.001). With increasing degrees of cervical lesions, the HPV16 infection rate (χ2=47.623, P<0.001), FHIT methylation rate (χ2=40.147, P<0.001) and the rate of FHIT protein low expression (χ2=65.098, P<0.001) were all gradually increasing. There appeared positive additive interaction between FHIT methylation, FHIT protein low expression and infection of HPV16. Conclusion Hypermethylation of FHIT gene, low expression of FHIT protein and HPV16 infection could increase the risk of cervical cancer and precancerous lesions. These results suggested that there might be synergistic action between FHIT gene hypermethylation and HPV16 infection in the progression of cervical cancer and the same was true between the low expression of FHIT protein and HPV 16 infection. |
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