Radiation exposure triggers the malignancy of non‑small cell lung cancer cells through the activation of visfatin/Snail signaling.
Radiation exposure triggers the malignancy of non‑small cell lung cancer cells through the activation of visfatin/Snail signaling.
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辐射暴露通过激活内脂素/Snail 信号传导引发非小细胞肺癌细胞的恶性
DOI：
10.3892/or.2021.7929
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发表时间：
2021-03
期刊：
影响因子：
4.2
通讯作者：
Wang F
中科院分区：
文献类型：
--
作者：
Xiao L;Mao Y;Tong Z;Zhao Y;Hong H;Wang F
据估计，全世界有一半的非小细胞肺癌（NSCLC）患者接受放疗。然而，单纯放疗的结果并不总是令人满意的。本研究的目的是评价放射治疗对非小细胞肺癌细胞恶性程度的影响。体外研究表明，放射治疗可增加NSCLC细胞的迁移和侵袭能力。此外，上调visfatin，52 kDa的脂肪因子，介导的辐射诱导的细胞运动。内脂素特异性中和抗体阻断辐射诱导的细胞迁移。放射和内脂素诱导Snail的表达，Snail是调节NSCLC细胞中上皮向间质转化的关键分子。内脂素对NSCLC细胞中Snail mRNA的稳定性有正向调节作用，但对Snail蛋白的降解无影响。这可能是由于内脂素介导的microRNA（miR）-34 a下调，其显示结合Snail mRNA的3′非翻译区以促进其衰变。总的来说，这些发现表明辐射可以通过内脂素/Snail信号传导诱导NSCLC细胞的细胞运动。
It is estimated that one-half of patients with non-small cell lung cancer (NSCLC) undergo radiotherapy worldwide. However, the outcome of radiotherapy alone is not always satisfactory. The aim of the present study was to evaluate the effects of radiotherapy on the malignancy of NSCLC cells. It was demonstrated that radiation therapy could increase the migration and invasion of NSCLC cells in vitro. Moreover, the upregulation of visfatin, a 52-kDa adipokine, mediated radiation-induced cell motility. A neutralizing antibody specific for visfatin blocked radiation-induced cell migration. Radiation and visfatin induced the expression of Snail, a key molecule that regulates epithelial to mesenchymal transition in NSCLC cells. Furthermore, visfatin positively regulated the mRNA stability of Snail in NSCLC cells, but had no effect on its protein degradation. This may be explained by visfatin-mediated downregulation of microRNA (miR)-34a, which was shown to bind the 3′ untranslated region of Snail mRNA to promote its decay. Collectively, these findings suggested that radiation could induce cell motility in NSCLC cells through visfatin/Snail signaling.
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影响因子：
4.9
作者：
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作者：
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