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死亡相关蛋白激酶1、KLF4、6-氧-甲基鸟嘌呤-DNA甲基转移酶甲基化状态检测及与宫颈癌人乳头瘤病毒16感染的关系

Detection of methylation status of death-related protein kinase 1, KLF4 and O6-methylguanine-DNA methyltransferase and their relationships with humanpapillomavirus type 16

    摘要
  • 摘要:
      目的  检测宫颈癌组织死亡相关蛋白激酶1(DAPK1)、KLF4、6-氧-甲基鸟嘌呤-DNA甲基转移酶(MGMT)启动子区域甲基化状态，初步探讨其甲基化状态与宫颈癌人乳头瘤病毒16(HPV16)感染的关系。
      方法  选取宫颈癌患者103例为宫颈癌组，另选取同期年龄相匹配的慢性子宫颈炎患者110例为对照组。检测2组宫颈脱落组织DAPK1、KLF4、MGMT基因甲基化状态。通过人乳头瘤病毒检测HPV16感染情况，分析宫颈癌组织DAPK1、KLF4、MGMT基因甲基化与HPV16感染相关性。
      结果  与对照组相比，宫颈癌组患者HPV16感染阳性率升高，差异有统计学意义(P < 0.05); 与对照组相比，宫颈癌组DAPK1、KLF4、MGMT基因异常甲基化率升高，差异有统计学意义(P < 0.05)。分化程度低、TNM分期Ⅲ~Ⅳ期、有淋巴结转移及有远处转移患者宫颈癌组织DAPK1、KLF4、MGMT甲基化率高于分化程度高、中及TNM分期Ⅰ~Ⅱ、无淋巴结转移、无远处转移患者，差异有统计学意义(P < 0.05)。与HPV16感染阴性相比, HPV16感染阳性患者中APK1、KLF4、MGMT甲基化比例升高，差异有统计学意义(P < 0.05)。HPV16感染情况与APK1、KLF4、MGMT甲基化相关(r=0.454, 0.497, 0.307, P < 0.05)。
      结论  HPV16感染可能与APK1、KLF4、MGMT甲基化有关, HPV16感染可能通过影响APK1、RAR-β、MGMT基因甲基化促进宫颈癌的发展。

     

    Abstract:
      Objective  To detect the methylation status of death-related protein kinase 1 (DAPK1), KLF4 and O6-methylguanine-DNA methyltransferase (MGMT) promoter region in cervical cancer tissues, and to preliminarily explore the relationship between their methylation status and human papillomavirus type 16 (HPV16) infection of cervical cancer.
      Methods  A total of 103 patients with cervical cancer were selected as cervical cancer group, and another 110 patients of chronic cervicitis with matched age in the same period were selected as control group. The methylation status of DAPK1, KLF4 and MGMT genes in cervical exfoliated tissues of the two groups were detected. HPV16 infection was detected by human papillomavirus, and the correlations of DAPK1, KLF4 and MGMT gene methylation with HPV16 infection were analyzed.
      Results  Compared with the control group, the positive rate of HPV16 infection in cervical cancer group was significantly increased (P < 0.05); compared with the control group, the abnormal methylation rates of DAPK1, KLF4 and MGMT genes in cervical cancer group were significantly increased (P < 0.05). The methylation rates of DAPK1, KLF4 and MGMT in cervical cancer tissues in patients with low differentiation, TNM stage Ⅲ to Ⅳ, lymph node metastases and distant metastases were significantly higher than those in patients with moderate to high differentiation, TNM stage Ⅰ to Ⅱ, without lymph node metastasis and without distant metastasis (P < 0.05). Compared with the negative HPV16 infection, the methylation rates of DAPK1, KLF4 and MGMT in HPV16 positive patients were increased significantly (P < 0.05). HPV16 infection was associated with methylation of DAPK1, KLF4 and MGMT (r=0.454, 0.497 and 0.307, P < 0.05).
      Conclusion  HPV16 infection may be related to the methylation of DAPK1, KLF4 and MGMT. HPV16 infection may promote the development of cervical cancer by influencing methylation of DAPK1, KLF4 and MGMT genes.

     

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