实用肝脏病杂志 ›› 2021, Vol. 24 ›› Issue (2): 244-247.doi: 10.3969/j.issn.1672-5069.2021.02.024

• 肝癌 • 上一篇    下一篇

肝细胞癌患者血清癌基因和抑癌基因蛋白水平变化

陈少华, 吴哲, 魏志鸿, 陈鹏   

  1. 350001 福州市 联勤保障部队第900医院肝胆外科(陈少华,吴哲,魏志鸿);
    福建医科大学附属省肿瘤医院肝胆胰外科(陈鹏)
  • 收稿日期:2020-11-05 出版日期:2021-03-10 发布日期:2021-04-30
  • 通讯作者: 吴哲,E-mail:497672206@qq.com
  • 作者简介:陈少华,男,56岁,大学本科,主任医师
  • 基金资助:
    福建省科技厅自然科学基金资助项目(编号:2018J01185)

Serum oncogene and tumor suppressor gene levels in patients with hepatocellular carcinoma

Chen Shaohua, Wu Zhe, Wei Zhihong, et al   

  1. Department of Hepatobiliary Surgery,900th Hospital of Joint Logistics Support Force, Fuzhou 350001,Fujian Province, China
  • Received:2020-11-05 Online:2021-03-10 Published:2021-04-30

摘要: 目的 探讨肝细胞癌(HCC)患者血清常见的癌基因和抑癌基因水平变化。方法 2017年7月~2020年7月我院收治的慢性乙型肝炎患者40例,代偿期乙型肝炎肝硬化患者25例,失代偿期乙型肝炎肝硬化患者31例,HCC 患者50例和同期体检的健康人40例,采用ELISA法检测血清癌基因转化基因(N-ras)、增殖相关基因(C-myc)、成纤维细胞生长因子(FGF)2、丝/苏氨酸激酶(PLK)1和抑癌基因铁调素(hepcidin)、清道夫受体(SCAR)A5、细胞周期依赖性蛋白激酶抑制剂(P16)蛋白水平。结果 HCC组血清癌基因N-ras、C-myc、FGF2和PLK1蛋白水平分别为(17.9±2.4)pg/mL、(16.2±2.0)pg/mL、(19.0±3.2)pg/mL和(15.4±1.9)pg/mL,显著高于失代偿期肝硬化患者【分别为(10.3±1.4)pg/mL、(10.0±1.2)pg/mL、(10.2±1.4)pg/mL和(9.0±1.1)pg/mL,P<0.05】或代偿期肝硬化患者【分别为(9.9±1.2)pg/mL、(9.9±1.1)pg/mL、(10.0±1.3)pg/mL和(9.1±1.0)pg/mL,P<0.05】或慢性乙型肝炎患者【分别为(9.8±1.1)pg/mL、(9.7±1.1)pg/mL、(9.9±1.2)pg/mL和(9.0±1.0)pg/mL,P<0.05】或健康人【分别为(1.2±0.2)pg/mL、(1.1±0.1)pg/mL、(1.1±0.2)pg/mL和(0.9±0.1)pg/mL,P<0.05】;HCC患者血清hepcidin、SCARA5和P16蛋白水平分别为(1.1±0.3)pg/mL、(1.3±0.3)pg/mL和(1.7±0.4)pg/mL,显著低于失代偿期肝硬化患者【分别为(5.3±0.7)pg/mL、(7.2±1.1)pg/mL和(6.4±0.8)pg/mL,P<0.05】或代偿期肝硬化患者【分别为(5.6±0.8)pg/mL、(7.3±1.1)pg/mL和(6.3±0.8)pg/mL,P<0.05】或慢性乙型肝炎患者【分别为(5.4±0.7)pg/mL、(7.9±1.1)pg/mL和(6.5±1.0)pg/mL,P<0.05】或健康人【分别为(12.9±1.2)pg/mL、(14.4±1.3)pg/mL和(11.6±0.9)pg/mL,P<0.05】。结论 肝细胞癌患者血清癌基因水平升高,而抑癌基因水平降低,可能参与了HCC的发病过程,其临床意义仍有待探讨。

关键词: 肝细胞癌, 癌基因, 抑癌基因

Abstract: Objective The aim of this study was to investigate serum oncogene and tumor suppressor gene level changes in patients with hepatocellular carcinoma (HCC).Methods 40 patients with chronic hepatitis B (CHB), 25 patients with compensated hepatitis B liver cirrhosis (LC), 31 patients with decompensated hepatitis B LC, 50 patients with HCC and 40 healthy persons were enrolled in our hospital between July 2017 and July 2020, and serum oncogene transformation of participants (N-ras), proliferation related genes (C-myc), fibroblast growth factor (FGF) 2, silk/threonine kinase (PLK) 1 as well as tumor-suppressor genes iron element (hepcidin), scavenger receptors (SCAR) A5, and cell cycle dependent protein kinase inhibitor (P16) protein were detected by ELISA.Results Serum N-ras, C-myc, FGF2 and PLK1 levels in patients with HCC were (17.9±2.4)pg/mL, (16.2±2.0)pg/mL,(19.0±3.2)pg/mL and (15.4±1.9)pg/mL, all significantly higher than 【(10.3±1.4)pg/mL,(10.0±1.2)pg/mL,(10.2±1.4)pg/mL and (9.0±1.1)pg/mL, respectively, P<0.05】 in patients with decompensated LC or 【(9.9±1.2)pg/mL,(9.9±1.1)pg/mL,(10.0±1.3)pg/mL and (9.1±1.0)pg/mL, respectively,P<0.05】 in patients with compensated LC or 【(9.8±1.1)pg/mL,(9.7±1.1)pg/mL,(9.9±1.2)pg/mL and (9.0±1.0)pg/mL, respectively, P<0.05】 in patients with CHB or 【(1.2±0.2)pg/mL, (1.1±0.1)pg/mL, (1.1±0.2)pg/mL and (0.9±0.1)pg/mL, respectively, P<0.05】 in healthy persons; serum hepcidin, SCARA5 and P16 levels in patients with HCC were (1.1±0.3)pg/mL,(1.3±0.3)pg/mL and (1.7±0.4)pg/mL, all significantly lower than 【(5.3±0.7)pg/mL,(7.2±1.1)pg/mL and (6.4±0.8)pg/mL, respectively, P<0.05】 in patients with decompensated LC or 【(5.6±0.8)pg/mL,(7.3±1.1)pg/mL and (6.3±0.8)pg/mL, respectively, P<0.05】 in patients with compensated LC or 【(5.4±0.7)pg/mL,(7.9±1.1)pg/mL and (6.5±1.0)pg/mL, respectively, P<0.05】 in patients with CHB or 【(12.9±1.2)pg/mL, (14.4±1.3)pg/mL and (11.6±0.9)pg/mL, respectively, P<0.05】 in healthy individuals.Conclusion The up-regulation of N-ras, c-myc, FGF2 and PLK1 and down-regulation of hepcidin, scara5 and p16 occur in patients with HCC, which might be involved in the hepatocarcinogenesis.

Key words: Hepatoma, Oncogene, Tumor suppressor gene