Peroxiredoxin 1 is a tumor-associated antigen in esophageal squamous cell carcinoma.

Peroxiredoxin 1 is a tumor-associated antigen in esophageal squamous cell carcinoma.
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过氧化还原蛋白 1 是食管鳞状细胞癌中的肿瘤相关抗原

DOI:
10.3892/or.2013.2714
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发表时间:
2013-11
期刊:
影响因子:
4.2
通讯作者:
Zhang J
Zhang J
中科院分区:
医学3区
文献类型:
--
作者:
Ren P;Ye H;Dai L;Liu M;Liu X;Chai Y;Shao Q;Li Y;Lei N;Peng B;Yao W;Zhang J

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过氧化氧还蛋白1 (Prdx1)是一种抗氧化剂,在h2o2介导的细胞信号传导中起重要作用。我们先前使用蛋白质组学方法发现,Prdx1在食管鳞状细胞癌(ESCC)组织中的表达水平升高。由于过表达蛋白可诱导自身免疫反应,为了进一步研究ESCC患者血清是否对Prdx1具有免疫反应性,我们采用ELISA、western blotting和间接免疫荧光法对ESCC患者和正常人血清中Prdx1的自身抗体反应进行了评估。利用组织阵列载玻片免疫组化和癌细胞western blot分析Prdx1蛋白在ESCC组织和癌细胞中的表达谱。结果显示,ESCC患者血清Prdx1自身抗体阳性率为13.2%(9/68),而正常人血清Prdx1自身抗体阳性率为0%(0/89)。数据还显示,Prdx1在ESCC组织中的表达明显高于配对的邻近正常组织(P<0.05)。这些数据表明,Prdx1可能与食管恶性转化有关,并可能作为ESCC免疫诊断的生物标志物。
Peroxiredoxin 1 (Prdx1) is an antioxidant and plays an important role in H2O2-mediated cell signaling. We previously found that the expression level of Prdx1 was elevated in esophagus squamous cell carcinoma (ESCC) tissue using a proteomics approach. Since overexpressed protein can induce an autoimmune response, to further examine whether serum from ESCC patients exhibits immunoreactivity against Prdx1, autoantibody responses to Prdx1 were evaluated by ELISA, western blotting and indirect immunofluorescence assay in sera from patients with ESCC and normal individuals. Immunohistochemical study with tissue array slides and western blot analysis with cancer cell lines were also performed to analyze the protein expression profiles of Prdx1 in ESCC tissues and cancer cell lines. The results demonstrated that the positive rate of autoantibody against Prdx1 in ESCC sera was 13.2% (9/68), whereas this rate was 0% (0/89) in normal individuals. Data also showed that expression of Prdx1 was significantly increased in ESCC tissues when compared to expression in paired adjacent normal tissues (P<0.05). The data indicate that Prdx1 may contribute to malignant transformation of the esophagus, and may be used as a biomarker in the immunodiagnosis of ESCC.
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