甲状腺激素不活化维持癌症干细胞的维持和瘤发生在基底细胞癌中
Daniela Di Girolamo1, Emery Di Cicco2, Caterina Miro3
1Department of Biology, University of Naples Federico II, 80126, Naples, Italy; CEINGE-Biotecnologie Avanzate Scarl, Naples, Italy.
The Journal of investigative dermatology
|February 5, 2026
概括
甲状腺酶3型 (D3) 通过保护它们免受甲状腺激素 (TH) 影响,维持基底细胞癌 (BCC) 中的癌症干细胞 (CSC). 准D3/TH轴可能会抑制BCC瘤的进展.
科学领域:
- 在瘤学瘤学.
- 内分泌学 在内分泌学.
- 分子生物学分子生物学
背景情况:
- 瘤层次涉及癌症干细胞 (CSCs) 驱动的增殖,转移和复发.
- CSCs对传统疗法有抗性,这使得它们成为关键的治疗点.
- 甲状腺激素 (TH) 调节细胞增殖和分化,由神酶酶控制.
研究的目的:
- 调查Deiodinase Type 3 (D3) 在基底细胞癌 (BCC) 癌症干细胞中的作用.
- 确定D3/TH轴对CSC自我更新和瘤进展的影响.
主要方法:
- 结合了BCC的体内小鼠模型与人类样本分析.
- 在小鼠中利用了D3的遗传切除.
- 分析了CSC种群,干性标记物 (Sox9) 和TH诱导的亡/分化.
主要成果:
- 在最致瘤的BCC CSC亚群中表达D3.
- D3基因切除减少了CSC和关键的茎状标记物,如Sox9.
- TH治疗抑制了Sox9的表达,并减少了CSC池.
- D3在人类BCC CSC中得到了丰富.
结论:
- D3通过防止TH诱导的亡和分化来维持BCC CSC的瘤发生潜力.
- 准D3/TH轴是针对BCC CSC自我更新和瘤进展的潜在治疗策略.
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