No mutation effect of 50 Hz sinusoidal magnetic field on beta catenin gene phosphorylation site in N-methyl-N-nitrosourea (MNU) induced colon tumor model

IF 0.7 4区 生物学 Q4 BIOLOGY
Metin Budak, Mahmut Alp K ı l ı ç, T. Kalkan, H. Tuncel
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引用次数: 0

Abstract

The dysregulation of beta-catenin, a key regulator of cadherin-mediated cell adhesion and crucial for embryonic development and adult tissue processes, has been implicated in various cancers, including colon cancer. Meanwhile, there have been longstanding concerns about the potential carcinogenic effects of magnetic fields. In this study, we investigated the possible relationship between beta-catenin dysfunction and 50 Hz sinusoidal magnetic fields (SMF) using an animal model of N-methyl-N-nitrosourea (MNU)-induced rat colon tumors. To assess beta-catenin phosphorylation, genomic DNA was extracted from 58 samples using a commercial extraction kit, and the target gene region corresponding to an important phosphorylation site of beta-catenin was amplified via polymerase chain reaction (PCR). The amplified samples were subsequently analyzed using the single-strand conformation polymorphism (SSCP) method to detect any differences between the experimental groups. Surprisingly, our results revealed no significant differences in beta-catenin gene phosphorylation sites among the groups. These findings suggest that 50 Hz SMF exposure may not directly impact beta-catenin dysfunction in the context of MNU-induced rat colon tumors. Implications of these results and avenues for further research are discussed.
50 赫兹正弦磁场对 N-甲基-N-亚硝基脲(MNU)诱导的结肠肿瘤模型中 beta 连环素基因磷酸化位点无突变效应
β-catenin是由粘连蛋白介导的细胞粘附的关键调节因子,对胚胎发育和成人组织过程至关重要。与此同时,人们对磁场的潜在致癌效应的担忧由来已久。在本研究中,我们利用 N-甲基-N-亚硝基脲(MNU)诱导的大鼠结肠肿瘤动物模型,研究了 beta 连环素功能障碍与 50 赫兹正弦磁场(SMF)之间的可能关系。为了评估 beta-catenin磷酸化,使用商业提取试剂盒从 58 个样本中提取了基因组 DNA,并通过聚合酶链式反应(PCR)扩增了对应于 beta-catenin 重要磷酸化位点的目标基因区。随后,利用单链构象多态性(SSCP)方法对扩增后的样本进行分析,以检测实验组之间的差异。令人惊讶的是,我们的结果显示,各组之间的β-catenin基因磷酸化位点没有明显差异。这些发现表明,在 MNU 诱导的大鼠结肠肿瘤中,50 Hz SMF 暴露可能不会直接影响β-catenin 的功能障碍。本文讨论了这些结果的意义和进一步研究的途径。
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来源期刊
CiteScore
1.57
自引率
33.30%
发文量
84
审稿时长
6 months
期刊介绍: This journal, started in 1963, publishes full papers, notes and reviews in cell biology, molecular biology, genetic engineering, endocrinology, reproductive biology, immunology, developmental biology, comparative physiology, radiation biology, chronobiology, microbiology, pharmacology, toxicology and other biological fields including instrumentation and methodology. The papers having experimental design involving alteration and/or manipulation in biological system(s) providing insight into their functioning are considered for publication. Studies involving higher animals, human beings and of clinical nature are not encouraged for publication in the journal.
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