Variable modulation by cytokines and thiazolidinediones of the prototype Th1 chemokine CXCL10 in anaplastic thyroid cancer

详细信息	查看全文 | 推荐本文 |

• 作者：Alessandro Antonelli^a ; ^{alessandro.antonelli@med.unipi.it} ; Silvia Martina Ferrari^a ; ^{sm.ferrari@int.med.unipi.it} ; Poupak Fallahi^a ; ^{poupak@int.med.unipi.it} ; Simona Piaggi^b ; ^{simona.piaggi@dps.unipi.it} ; Andrea Di Domenicantonio^a ; ^{didomand@libero.it} ; David Galleri^c ; ^{galleridavid@hotmail.com} ; Libero Santarpia^d ; ^{lsantarpia@usl4.toscana.it} ; Fulvio Basolo^c ; ^{f.basolo@med.unipi.it} ; Ele Ferrannini^a ; ^{ferranni@ifc.cnr.it} ; Paolo Miccoli^c ; ^{p.miccoli@dc.med.unipi.it}
• 关键词：ANA ; primary ATC cells cultures ; ATC ; anaplastic thyroid cancer ; BCA ; bicinchoninic acid ; CXCL ; chemokine (C&ndash ; X&ndash ; C motif) ligand ; CXCR ; CXC chemokine receptors ; ELISA ; enzyme-linked immunosorbent assay ; EMA ; European medicine agency ; EMSA ; elect
• 刊名：Cytokine
• 出版年：2012
• 期刊代码：97_10434666
• 类别：imm
• 出版时间：August, 2012
• 卷：59
• 期：2
• 页码：218-222
• 文件大小：475 K

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 鈥減rimary human ATC cells鈥?(ANA) vs 鈥渘ormal thyroid follicular cells鈥?(TFC): (a) CXCL10 secretion basally and after interferon (IFN)-纬 and/or tumor necrosis factor (TNF)-伪 stimulation; (b) peroxisome proliferator-activated receptor (PPAR)-纬 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-纬 stimulated dose-dependently CXCL10, in ANA and TFC; (c) TNF-伪 did not induce CXCL10 secretion, in ANA and TFC; (d) IFN-纬 + TNF-伪 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-魏B and ERK1/2 were basally activated in ANA, increased by IFN-纬 + TNF-伪, 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-纬, TNF-伪 or thiazolidinediones is extremely variable, suggesting that the intracellular pathways involved in the chemokine modulation in ATC have different types of deregulation.