甲状腺激素的激活调节了乳腺癌和甲状腺干细胞之间的交叉声
Annarita Nappi1, Vittoria D'Esposito2,3, Caterina Miro1
1Department of Clinical Medicine and Surgery, University of Naples "Federico II", 80131 Naples, Italy.
甲状腺激素 (THs) 通过D2酶激活乳腺癌细胞,促进它们的入侵和与介质干细胞 (MSCs) 的相互作用. 阻止D2可能是乳腺癌治疗的新疗法策略.
科学领域:
- 内分泌学 在内分泌学.
- 在瘤学瘤学.
- 细胞生物学 细胞生物学
背景情况:
- 甲状腺激素 (THs) 在癌症中起着双重作用,过量与增加瘤生长有关.
- 乳腺癌的进展涉及瘤细胞和瘤微环境之间的复杂相互作用,包括介质干细胞 (MSC).
- 通过强大的瘤原源性活动,MSCs有助于瘤进展.
研究的目的:
- 为了研究THs在调节乳腺癌中瘤-肌瘤交叉的作用.
- 确定D2酶活性对乳腺癌细胞行为和与MSCs相互作用的影响.
主要方法:
- 人类MSC与野生类型 (WT) 和DIO2敲除 (D2KO) MCF7乳腺癌细胞的共同培养.
- 细胞生长,迁移,入侵和上皮层-介质细胞过渡 (EMT) 标志物的评估.
- 采用了老鼠-输入管内 (MIND) 注射模型进行体内瘤特征.
主要成果:
- MCF7细胞通过D2激活细胞内THs,增强EMT和MSC通信.
- 在MCF7细胞中D2无活化降低了侵入性和MSC诱导的前瘤原生效应.
- 这些发现在体外和体内均一致.
结论:
- 细胞内TH激活D2对于乳腺癌细胞的侵入性和转移性潜力至关重要.
- 阻止D2是乳腺癌治疗的潜在治疗策略.
- 准D2可能会破坏瘤-肌瘤相互作用,并抑制癌症的进展.
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