Effect of the micronutrient iodine in thyroid carcinoma angiogenesis.
Effect of the micronutrient iodine in thyroid carcinoma angiogenesis.
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微量营养素碘在甲状腺癌血管生成中的影响。
DOI：
10.18632/aging.101143
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发表时间：
2016-12-20
期刊：
影响因子：
--
通讯作者：
Nucera C
中科院分区：
文献类型：
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作者：
Daniell K;Nucera C
碘是一种微量营养素，对甲状腺激素的产生至关重要。甲状腺细胞对碘的摄取和代谢对正常的甲状腺功能至关重要。碘离子通过细胞膜中的钠碘同向转运体(NIS)进入甲状腺滤泡细胞，并结合到酪氨酸残基中，最终形成甲状腺激素。我们试图了解甲状腺细胞内异常浓度的碘如何对甲状腺，特别是周围的血管网络产生显著影响。碘水平不足会导致多种途径的表达或活性增加，包括血管内皮生长因子(VEGF)。血管内皮生长因子蛋白促进血管生长(血管生成)，从而增强周围细胞可获得的营养物质。或者，正常/过剩的碘水平可能会对血管生成产生抑制作用。甲状腺中不同水平的碘可以通过调节缺氧诱导因子-1(HIF-1)和血管内皮生长因子(VEGF)依赖的途径来影响甲状腺癌细胞的增殖和血管生成。我们回顾了一些研究，以探讨碘对血管生成和氧化应激调节的影响如何影响甲状腺癌细胞的活性。概述的各种研究对碘在甲状腺滤泡功能和血管生长中的作用提供了关键的见解，总体上强调了不足的碘水平刺激导致血管生长的途径，反之亦然，正常/过剩的碘水平抑制了这些途径。有趣的是，促甲状腺激素和碘水平不同地调节血管生成因子的表达水平。包括癌细胞在内的所有细胞都会增加对血液营养物质的摄取，这意味着血管轮廓对肿瘤的生长和进展有影响。重要的是，碘浓度的变化也会影响BRAFV600E介导的致癌活性，并可能放松对肿瘤增殖的调控。尽管这些机制尚未得到很好的阐明，但碘浓度和代谢可能通过调控不同的分子途径对甲状腺癌细胞的活力产生重要影响，包括血管生成调节自分泌和微环境介导的信号。
Iodide is a micronutrient essential for thyroid hormone production. The uptake and metabolism of iodide by thyrocytes is crucial to proper thyroid function. Iodide ions are drawn into the thyroid follicular cell via the sodium-iodide symporter (NIS) in the cell membrane and become integrated into tyrosyl residues to ultimately form thyroid hormones. We sought to learn how an abnormal concentration of iodide within thyrocyte can have significant effects on the thyroid, specifically the surrounding vascular network. Insufficient levels of iodide can lead to increased expression or activity of several pathways, including vascular endothelial growth factor (VEGF). The VEGF protein fuel vessel growth (angiogenesis) and therefore enhances the nutrients available to surrounding cells. Alternatively, normal/surplus iodide levels can have inhibitory effects on angiogenesis. Varying levels of iodide in the thyroid can influence thyroid carcinoma cell proliferation and angiogenesis via regulation of the hypoxia inducible factor-1 (HIF-1) and VEGF-dependent pathway. We have reviewed a number of studies to investigate how the effect of iodide on angiogenic and oxidative stress regulation can affect the viability of thyroid carcinoma cells. The various studies outlined give key insights to the role of iodide in thyroid follicles function and vascular growth, generally highlighting that insufficient levels of iodide stimulate pathways resulting in vascular growth, and viceversa normal/surplus iodide levels inhibit such pathways. Intriguingly, TSH and iodine levels differentially regulate the expression levels of angiogenic factors. All cells, including carcinoma cells, increase uptake of blood nutrients, meaning the vascular profile is influential to tumor growth and progression. Importantly, variation in the iodine concentrations also influence BRAFV600E-mediated oncogenic activity and might deregulate tumor proliferation. Although the mechanisms are not well eluted, iodine concentrations and metabolism might have a crucial influence on thyroid carcinoma cell viability via regulation of different molecular pathways, including angiogenesis regulatory autocrine and microenvironment-mediated signals.