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目的探讨过氧化物酶1(Prx 1)在肝癌形成和恶性进展中的作用。方法蛋白质印迹法(Western blot)检测远癌肝组织和近癌肝组织中Prx 1、p Akt及Akt表达差异。肝细胞饥饿培养24 h后,10 ng/ml表皮生长因子(EGF)处理10 min,提取总蛋白,Western blot检测Prx 1、p Akt、不同位点磷酸化表皮生长因子受体(EGFR)和总EGFR。Western blot检测检测未处理组、转染无义sh RNA组及转染Prx 1 sh RNA组Hep G2细胞中Prx 1蛋白的表达。DCFH-DA法检测3种Hep G2细胞中活性氧簇总量。转染无义sh RNA组及转染Prx 1sh RNA组Hep G2细胞皮下注射至SCID小鼠,注射后每周测量1次皮下肿瘤体积。Western blot检测两组小鼠皮下肿瘤组织中Prx 1和p Akt的表达情况。结果与正常肝细胞比较,Prx 1在肝转化细胞中表达升高。Prx1增强了EGF介导的EGFR和Akt激活。Prx 1表达沉默抑制了Hep G2体内成瘤能力。减少Hep G2皮下移植瘤的肝转移。Prx 1表达沉默还抑制了Akt体内激活。结论 Prx 1具有调控人肝细胞中EGFR介导信号通路的潜在作用。Prx 1能够通过EGFR-Akt信号通路介导细胞正常至异常转化、肿瘤形成及转移
Objective To investigate the role of peroxiredoxin 1 (Prx 1) in the formation and progression of hepatocellular carcinoma. Methods Western blot was used to detect the expression of Prx 1, p Akt and Akt in distantly advanced liver tissues and near-cancer liver tissues. Twenty-four hours after hepatocyte starvation culture, 10 ng / ml epidermal growth factor (EGF) was treated with 10 ng / ml EGF for total protein extraction. Prx 1, p Akt, phosphorylated epidermal growth factor receptor EGFR. The protein expression of Prx 1 in untreated, transfected non-sense sh RNA and Hep G2 cells transfected with Prx 1 sh RNA were detected by Western blot. The total amount of reactive oxygen species in three kinds of Hep G2 cells was detected by DCFH-DA method. Transfection of nonsense sh RNA group and Hep G2 cells transfected with Prx 1sh RNA group were subcutaneously injected into SCID mice, and the subcutaneous tumor volume was measured once a week after injection. Western blot was used to detect the expression of Prx 1 and p Akt in the subcutaneous tumor of the two groups. Results Compared with normal hepatocytes, Prx 1 expression increased in liver transformed cells. Prx1 enhances EGF-mediated EGFR and Akt activation. Silencing Prx 1 expression inhibits Hep G2 tumorigenicity in vivo. Reduce Hep G2 subcutaneous xenograft liver metastases. Silencing Prx 1 also inhibits Akt in vivo activation. Conclusion Prx 1 has a potential role in regulating EGFR-mediated signaling in human hepatocytes. Prx 1 mediates normal to abnormal cell transformation, tumor formation and metastasis through the EGFR-Akt signaling pathway