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介质素-6促进了乳头甲状腺癌细胞的脱差

Guo-Qiang Zhang¹, Chuang Xi¹, Chen-Tian Shen¹

¹Department of Nuclear Medicine, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China.

Endocrine-related cancer

|June 1, 2023

概括

干乐素-6 (IL-6) 降低了皮肤状甲状腺癌 (PTC) 细胞中的/合载体 (NIS) 表达,阻碍了放射性治疗的疗效. 这项研究揭示了IL-6激活了抑制PTC中NIS转录的信号通路.

科学领域:

在瘤学瘤学.
分子生物学分子生物学
内分泌学在内分泌学.

背景情况:

放射性治疗对于乳头甲状腺癌 (PTC) 治疗至关重要.
/合载体 (NIS) 表达对于放射性的吸收和治疗的有效性至关重要.
瘤前导细胞因子 - - 干白素-6 (IL-6) 在调节NIS在PTC中的表达中的作用尚不清楚.

研究的目的:

调查IL-6对NIS表达和放射性治疗在PTC中的疗效的影响.
阐明IL-6在PTC细胞中影响NIS表达的分子机制.

主要方法:

进行了细胞增殖试验.
对NIS和其他甲状腺特异性基因和转录因子表达进行了定量分析.
使用特定途径抑制剂 (MAPK,JAK) 和基因枯竭 (c-Jun,STAT3) 的抑制研究被采用.
使用转录因子 (TTF-1,PAX-8) 的过度表达和用IL-6受体阻断剂 (托西利祖马布) 的治疗.

主要成果:

IL-6增强了PTC细胞增殖,并且与甲状腺癌组织中的NIS表达负相关.
IL-6降低了NIS,甲状腺过氧化酶和甲状腺刺激激素受体,以及TTF-1和PAX-8转录因子的调节.
基激活蛋白激酶 (MAPK) 和Janus激酶 (JAK) 途径的抑制剂,以及c-Jun和STAT3的耗尽,挽救了IL-6诱导的NIS下调.
在恢复NIS,TTF-1和PAX-8表达方面,STAT3枯竭显示出比c-Jun枯竭更显著的效果.
过度表达TTF-1和PAX-8挽救了由IL-6诱导的NIS下调.
托西利祖马布阻断了IL-6对NIS表达的抑制作用,而不影响PTC细胞的增殖或分化.

结论:

IL-6 抑制 PTC 细胞中的 NIS 转录,主要通过激活 MAPK 和 JAK 信号通路.
STAT3和c-Jun是IL-6诱导的NIS和相关的转录因子降低调节的关键媒介.
针对IL-6信号传递可能提供一种策略,通过恢复NIS表达来提高PTC中放射性治疗的疗效.

关键词:

没有分化,没有分化.介质蛋白-6 介质蛋白-6 是一种皮囊性甲状腺癌是什么?/化物是同载体.

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