| 徐金锴,李宗禹,苏清华,赵 军,马建仓.甲状腺乳头状癌中TLR4对Foxp3表达的调控作用分析[J].,2017,17(14):2635-2639 |
| 甲状腺乳头状癌中TLR4对Foxp3表达的调控作用分析 |
| Regulation Analysis of Foxp3 Expression by TLR4 in Papillary Thyroid Carcinoma |
| 投稿时间：2016-06-30 修订日期：2016-07-23 |
| DOI：10.13241/j.cnki.pmb.2017.14.008 |
| 中文关键词: 甲状腺乳头状癌 Toll样受体4 叉头蛋白3 脂多糖 |
| 英文关键词: Papillary thyroid carcinoma TLR4 Foxp3 Lipopolysaccharide |
| 基金项目: |
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| 中文摘要: |
| 摘要 目的：探讨人甲状腺乳头状癌（PTC）细胞中TLR4信号通路对Foxp3表达的调控作用。方法：以人甲状腺乳头状癌K1细胞株为实验材料，选用脂多糖(LPS)作为配体来激活TLR4信号通路，采用RT-PCR方法检测LPS在不同浓度（0, 5, 10, 20, 40 μg/mL）和不同时间点（12, 24, 36, 48 h）Foxp3的mRNA表达量，流式细胞术检测相应浓度和时间点的Foxp3蛋白和TLR4蛋白表达量的变化；加入LPS抑制剂多粘菌素B（PMB）后Foxp3和mRNA和蛋白的表达量分别利用RT-PCR和流式细胞术检测。结果：10 μg/mL的LPS可以显著上调PTC细胞中Foxp3 mRNA和蛋白的表达量（P<0.05），在第24小时达到最佳；LPS作用下，TLR4表达量上调；PMB阻断TLR4信号通路后，Foxp3蛋白表达量较未阻断组显著降低（P<0.05）。结论：在甲状腺乳头状癌K1细胞株中，TLR4作为上游信号调控因子，通过自身表达量改变，进而参与调控Foxp3的表达。 |
| 英文摘要: |
| ABSTRACT Objective: To investigate whether the expression of Foxp3 in human's Papillary thyroid carcinoma (PTC) cells could be regulated by TLR4 signaling pathway activation. Methods: We used human's thyroid carcinoma K1 cells as the research object, and choose lipopolysaccharide (LPS) as a ligand to activate TLR4 signaling pathway. The mRNA expression level of Foxp3 was detected by RT-PCR method in different LPS concentrations (0, 5, 10, 20, 40 μg/mL) and at different time points (12, 24, 36, 48 h). The protein expression level of Foxp3 and TLR4 were detected by flow cytometry. The expression level of Foxp3 mRNA and protein were detected by RT-PCR and flow cytometry respectively after adding LPS inhibitor polymyxin B (PMB). Results: The mRNA level of Foxp3 was significantly increased by 10 μg/mL LPS at 24 hours (P<0.05). And the protein level of TLR4 was significantly increased by LPS activation. After the PMB blocking TLR4 signaling pathway, the expression of Foxp3 mRNA and protein were significantly decreased than that of without blocking group (P<0.05). Conclusion: In human's Papillary thyroid carcinoma (PTC) K1 cells, TLR4 as the upstream signaling molecules, it could be involved in regulation of Foxp3 by its own expression changed. |
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