结直肠癌中锰超氧化物歧化酶（MnSOD）和谷胱甘肽过氧化物酶1（GPX1）基因表达及血清水平的测定
Determination of gene expression and serum levels of MnSOD and GPX1 in colorectal cancer.
作者信息
Nalkiran Ihsan, Turan Saime, Arikan Soykan, Kahraman Özlem Timirci, Acar Leyla, Yaylim Ilhan, Ergen Arzu
机构信息
Faculty of Medicine, Department of Medical Biology, Recep Tayyip Erdogan University, Rize, Turkey.
Department of Molecular Medicine, Institute of Experimental Medicine, Istanbul University, Istanbul, Turkey.
出版信息
Anticancer Res. 2015 Jan;35(1):255-9.
BACKGROUND/AIM: Oxidative stress plays a role on the development of colorectal cancer. Manganese superoxide dismutase (MnSOD) and glutathione peroxidase 1 (GPX1) are crucial in regulating oxidative balance and its stabilization. Possible mechanisms of action of these enzymes in various types of cancers require further investigation. We aimed to determine expression levels of these genes and their effects on protein levels in serum of patients with colorectal cancer.
MATERIALS AND METHODS
Expression levels of genes were determined using Real Time-Polymerase chain reaction in 35 patients with colorectal cancer. We used enzyme-linked immunosorbent assay to determine MnSOD and GPX1 levels.
RESULTS
We found significant differences in GPX1 expression between tumor and normal tissues, with a 2-fold decrease in tumor tissues (p<0.05). However, although no significant difference was found between the expression of MnSOD gene in tumor and that in normal tissues, there was a 1.13-fold change in expression. We observed no relationship between expressions of either gene and their levels in serum.
CONCLUSION
The GPX1 gene may play a critical role in the development of colorectal cancer.
背景/目的：氧化应激在结直肠癌的发生发展中起作用。锰超氧化物歧化酶（MnSOD）和谷胱甘肽过氧化物酶1（GPX1）在调节氧化平衡及其稳定方面至关重要。这些酶在各类癌症中的可能作用机制需要进一步研究。我们旨在确定这些基因在结直肠癌患者血清中的表达水平及其对蛋白质水平的影响。
材料与方法
采用实时聚合酶链反应测定35例结直肠癌患者的基因表达水平。我们使用酶联免疫吸附测定法来测定MnSOD和GPX1水平。
结果
我们发现肿瘤组织与正常组织之间的GPX1表达存在显著差异，肿瘤组织中降低了2倍（p<0.05）。然而，尽管肿瘤组织和正常组织中MnSOD基因的表达未发现显著差异，但表达有1.13倍的变化。我们未观察到任一基因的表达与其血清水平之间存在关联。
结论
GPX1基因可能在结直肠癌的发生发展中起关键作用。
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