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使用单细胞转录组学探索哈西莫托甲状腺炎炎炎症癌症转化背后的分子机制
Mengsha Zou1, Shang Shi1, Huihui Li1
1Thyroid Department, The Affiliated Lihuili Hospital of Ningbo University, Ningbo City, Zhejiang Province, P. R. China.
Autoimmunity
|March 11, 2026
概括
哈西莫托甲状腺炎 (HT) 炎症驱动乳头甲状腺癌 (PTC) 通过IL1B阴性毛囊上皮细胞招募雄性腺细胞. 然后,母细胞IL-8激活PI3K/AKT通路,促进癌症的发展.
科学领域:
- 在瘤学瘤学.
- 免疫学 免疫学 免疫学
- 细胞生物学 细胞生物学
背景情况:
- 哈西莫托甲状腺炎 (HT) 与乳头甲状腺癌 (PTC) 的发展有关.
- 在HT-PTC中,瘤免疫微环境和炎症转化为癌症的机制尚不清楚.
研究的目的:
- 研究在HT-PTC共存中驱动炎症转化为癌症的分子机制.
- 识别关键的细胞相互作用和涉及的信号通路.
主要方法:
- 单细胞RNA测序 (scRNA-seq) 的HT和PTC组织.
- 复制数变异 (CNV) 分析以识别恶性细胞.
- 使用Transwell共同培养模型进行细胞与细胞通信分析和体外验证.
主要成果:
- 确定了11种细胞亚型,IL1B在恶性毛囊上皮细胞 (FECs) 中被上调.
- 阴性IL1B的FEC通过FN1/CD44轴与巨细胞进行通信.
- 巨细胞分泌IL-8,激活PI3K/AKT通路,并在炎症下促进恶性表型.
结论:
- 阴性IL1B的FEC通过FN1/CD44轴招募巨细胞.
- 来自母细胞的IL-8激活PI3K/AKT通路,驱动HT转变为PTC.
- 为HT-PTC中炎症转化为癌症的机制提供了新的见解.
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