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首页> 外文期刊>Cytokine >TNFalpha induces chromosomal abnormalities independent of ROS through IKK, JNK, p38 and caspase pathways.
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TNFalpha induces chromosomal abnormalities independent of ROS through IKK, JNK, p38 and caspase pathways.

机译：TNFalpha通过IKK，JNK，p38和caspase途径诱导独立于ROS的染色体异常。

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A role for pro-inflammatory cytokines in inflammation-related cancers has been suggested, but mechanisms are not defined. Here, we demonstrate that treatment of HeLa cells with TNFalpha increases chromosomal aberration. In contrast, IL-1beta did not increase, but rather decreased chromosomal aberration. TNFalpha and IL-1beta increased the production of H2O2 to similar levels in cells, suggesting that increased production of reactive oxygen species might not be the premier factor involved. Reducing H2O2 through overexpression of catalase or treatment of cells with NAC or BHA did not have an effect on TNF-induced chromosomal aberration. TNFalpha-induced NO production has been implicated in DNA damage. Inhibiting NO did not reduce TNF-induced chromosomal aberration. Inhibiting IKK, JNK, and p38 kinase as well as caspases decreased TNF-induced chromosomal aberration, and a correlation between TNF-induced apoptosis and CA generation was not found. Single-strand DNA breaks give rise to double-strand breaks, which then results in chromosomal breaks, when replication forks reach the single-strand breaks during S-phase. In cells progressing through S-phase, TNFalpha activation of IKK, JNK, and p38 is significantly reduced. However, these kinases were activated by IL-1beta in S-phase. The possibility that these pathways, in a TNF-specific manner, may regulate either the generation of single- and double-strand breaks or their repair, thereby resulting in increased chromosomal aberration, is discussed.
机译：已经提出了促炎细胞因子在与炎症相关的癌症中的作用，但是尚未定义机制。在这里，我们证明用TNFα治疗HeLa细胞会增加染色体畸变。相反，IL-1β没有增加，而是减少了染色体畸变。 TNFalpha和IL-1beta将H2O2的产生增加到细胞中的相似水平，这表明活性氧产生的增加可能不是所涉及的主要因素。通过过氧化氢酶的过表达或用NAC或BHA处理细胞来减少H2O2对TNF诱导的染色体畸变没有影响。 TNFalpha诱导的NO产生与DNA损伤有关。抑制NO并不能降低TNF诱导的染色体畸变。抑制IKK，JNK和p38激酶以及胱天蛋白酶可降低TNF诱导的染色体畸变，并且未发现TNF诱导的细胞凋亡与CA生成之间存在相关性。当复制叉在S期达到单链断裂时，单链DNA断裂会引起双链断裂，然后导致染色体断裂。在经历S期的细胞中，IKK，JNK和p38的TNFalpha激活显着降低。但是，这些激酶在S期被IL-1β激活。讨论了这些途径以TNF特异性方式可能调节单链和双链断裂的产生或其修复，从而导致染色体畸变增加的可能性。

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