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Methylation degree of metalloproteinase inhibitor RECK gene: Links to RECK protein level and hepatocellular carcinoma in chronic HCV infection patients
Journal of Biochemical and Molecular Toxicology ( IF 3.2 ) Pub Date : 2021-08-15 , DOI: 10.1002/jbt.22886
Salwa M Abo El-Khair 1 , Hatem Elalfy 2 , Muhammad Diasty 2 , Eman E Ebrahim 2 , Ayman Z Elsamanoudy 1, 3
Affiliation  

The RECK gene, a tumor suppressor gene, inhibits angiogenesis, invasion, and tumor metastasis. Epigenetic regulation of the RECK gene constitutes a potent approach to the molecular basis of liver malignancy. This study aims to evaluate the promoter methylation status of the RECK gene and its serum level in patients with hepatitis C virus (HCV)-related hepatocellular carcinoma (HCC) and the potential association of RECK gene methylation with clinical criteria of HCC. One hundred and fifty-five subjects were included (healthy control [55], chronic HCV patients [55], HCV-related HCC patients [45]). The methylation status of the RECK gene promoter and serum RECK level were investigated by methylation-specific PCR and enzyme-linked immunosorbent assay techniques, respectively. RECK gene promoter hypermethylation was recorded in 46.7% of HCC patients, and 10.9% of HCV patients, but not in control subjects (0%). It was related to RECK protein level, varices, edema, ascites, lymph node metastasis, vascular invasion, and the largest diameter of focal lesions. Meanwhile, it was not associated with focal lesion number nor distant metastasis of HCC. In conclusion, RECK gene promoter hypermethylation is linked to HCV genotype-4-related HCC. Moreover, different degrees of RECK gene promoter methylation are associated with serum RECK level, lymph node metastasis, and vascular invasion, which could prove its pathogenic role in hepatocarcinogenesis in chronic HCV-infected patients.

中文翻译:

金属蛋白酶抑制剂 RECK 基因的甲基化程度:与慢性 HCV 感染患者的 RECK 蛋白水平和肝细胞癌有关

RECK基因是一种肿瘤抑制基因,可抑制血管生成、侵袭和肿瘤转移。RECK 基因的表观遗传调控构成了研究肝脏恶性肿瘤分子基础的有效方法。本研究旨在评估丙型肝炎病毒(HCV)相关肝细胞癌(HCC)患者的RECK基因启动子甲基化状态及其血清水平,以及RECK基因甲基化与HCC临床标准的潜在关联。包括 155 名受试者(健康对照组 [55]、慢性 HCV 患者 [55]、HCV 相关 HCC 患者 [45])。分别通过甲基化特异性 PCR 和酶联免疫吸附测定技术研究 RECK 基因启动子的甲基化状态和血清 RECK 水平。在 46.7% 的 HCC 患者中记录到 RECK 基因启动子高甲基化,和 10.9% 的 HCV 患者,但在对照组中没有 (0%)。与RECK蛋白水平、静脉曲张、水肿、腹水、淋巴结转移、血管侵犯、病灶最大直径有关。同时,它与HCC的病灶数量和远处转移无关。总之,RECK 基因启动子高甲基化与 HCV 基因型 4 相关的 HCC 相关。此外,不同程度的 RECK 基因启动子甲基化与血清 RECK 水平、淋巴结转移和血管侵犯有关,这可以证明其在慢性 HCV 感染患者肝癌发生中的致病作用。它与HCC的局灶性病变数量和远处转移无关。总之,RECK 基因启动子高甲基化与 HCV 基因型 4 相关的 HCC 相关。此外,不同程度的 RECK 基因启动子甲基化与血清 RECK 水平、淋巴结转移和血管侵犯有关,这可以证明其在慢性 HCV 感染患者肝癌发生中的致病作用。它与HCC的局灶性病变数量和远处转移无关。总之,RECK 基因启动子高甲基化与 HCV 基因型 4 相关的 HCC 相关。此外,不同程度的 RECK 基因启动子甲基化与血清 RECK 水平、淋巴结转移和血管侵犯有关,这可以证明其在慢性 HCV 感染患者肝癌发生中的致病作用。
更新日期:2021-10-15
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