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首页> 外文期刊>Cytokine >Variable modulation by cytokines and thiazolidinediones of the prototype Th1 chemokine CXCL10 in anaplastic thyroid cancer
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Variable modulation by cytokines and thiazolidinediones of the prototype Th1 chemokine CXCL10 in anaplastic thyroid cancer

机译：Th1型趋化因子CXCL10原型在变性甲状腺癌中的细胞因子和噻唑烷二酮的可变调节作用

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摘要

Until now, no data are present in literature about the prototype Th1 chemokine (C-X-C motif) ligand 10 (CXCL10) in anaplastic thyroid cancer (ATC).This study aimed to test in "primary human ATC cells" (ANA) vs "normal thyroid follicular cells" (TFC): (a) CXCL10 secretion basally and after interferon (IFN)-γ and/or tumor necrosis factor (TNF)-α stimulation; (b) peroxisome proliferator-activated receptor (PPAR)-γ activation by thiazolidinediones, rosiglitazone or pioglitazone, on CXCL10 secretion, on proliferation and apoptosis in ANA. We demonstrate that: (a) ANA, but not TFC, produced basally CXCL10, and did so in half of cases; (b) IFN-γ stimulated dose-dependently CXCL10, in ANA and TFC; (c) TNF-α did not induce CXCL10 secretion, in ANA and TFC; (d) IFN-γ + TNF-α induced a synergistic but variable release of CXCL10 in the different ANA preparations, while it was more reproducible in TFC; (e) rosiglitazone action on CXCL10 in ANA was inhibitory in 2/6, stimulatory in 1/6 and nil in 3/6, whereas it was inhibitory in TFC; (f) rosiglitazone inhibition of proliferation in ANA was not associated with the effect on CXCL10; (g) nuclear factor-κB and ERK1/2 were basally activated in ANA, increased by IFN-γ + TNF-α, and rosiglitazone inhibited that activation. On the whole, the present data first show that ANA cells are able to produce CXCL10, basally and under the influence of cytokines. However, the pattern of modulation by IFN-γ, TNF-α or thiazolidinediones is extremely variable, suggesting that the intracellular pathways involved in the chemokine modulation in ATC have different types of deregulation.
机译：到目前为止，关于变性变性甲状腺癌（ATC）中原型Th1趋化因子（CXC基序）配体10（CXCL10）的文献资料尚无。该研究旨在测试“原代人ATC细胞”（ANA）与“正常甲状腺”卵泡细胞”（TFC）：( a）干扰素（IFN）-γ和/或肿瘤坏死因子（TNF）-α刺激后基础分泌CXCL10; （b）噻唑烷二酮，罗格列酮或吡格列酮对过氧化物酶体增殖物激活受体（PPAR）-γ的激活对CXCL10分泌，ANA中增殖和凋亡的影响。我们证明：（a）ANA，而不是TFC，基本生产CXCL10，并且在一半情况下生产; （b）在ANA和TFC中，IFN-γ剂量依赖性地刺激了CXCL10; （c）TNF-α在ANA和TFC中不诱导CXCL10分泌; （d）IFN-γ+TNF-α在不同的ANA制剂中诱导了协同但可变的CXCL10释放，而在TFC中更具有重现性; （e）罗格列酮对ANA中CXCL10的作用是抑制2/6，刺激性是1/6，无刺激是3/6，而它在TFC中是抑制性的; （f）罗格列酮对ANA中增殖的抑制与对CXCL10的影响无关; （g）核因子-κB和ERK1 / 2在ANA中被基本激活，被IFN-γ+TNF-α增强，而罗格列酮抑制了该激活。总体而言，目前的数据首先表明，ANA细胞能够在细胞因子的基础上产生CXCL10。但是，IFN-γ，TNF-α或噻唑烷二酮类药物的调节模式极为不同，这表明参与ATC趋化因子调节的细胞内途径有不同类型的失调。

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