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人体脂肪衍生干细胞通过勒素通路促进皮皮性甲状腺癌细胞的迁移
Bo-Tao Zhang1,2, Ying Li1, Qi-Lan Jiang3
1Department of General Surgery (Thyroid Surgery), The Affiliated Hospital of Southwest Medical University, Luzhou, China.
Annals of medicine
|October 25, 2024
概括
人体脂肪衍生干细胞 (ADSCs) 通过通过勒普丁上调矩阵金属蛋白酶2 (MMP-2) 来促进甲状腺癌细胞的入侵和迁移. 这一发现可能解释了肥胖如何增加甲状腺癌的侵袭性.
科学领域:
- 在瘤学瘤学.
- 干细胞生物学 干细胞生物学
- 内分泌学 在内分泌学.
背景情况:
- 肥胖与增加甲状腺癌发病率和较差的结果有关.
- 连接肥胖和甲状腺癌进展的潜在机制仍然不清楚.
- 人类脂肪衍生干细胞 (ADSC) 参与各种生物过程,包括癌症.
研究的目的:
- 研究ADSCs对甲状腺癌细胞入侵和迁移的影响.
- 阐明丁在调解ADSC诱导的甲状腺癌细胞影响中的作用.
- 探索减轻与肥胖相关的甲状腺癌进展的潜在治疗点.
主要方法:
- 培养的甲状腺癌细胞系 (TPC-1,BCPAP) 与ADSCs受条件介质 (ADSC-CM).
- 评估细胞增殖 (CCK8,EDU) 和迁移 (Transwell,伤口关闭试验).
- 在体外和体内 (裸体小鼠异种移植模型) 使用了素中和抗体 (NAB) 和alo-aca (素受体对手).
主要成果:
- ADSC-CM显著增强了甲状腺癌细胞的入侵和迁移,增加了矩阵金属蛋白酶2 (MMP-2) 水平.
- 瘦素阻断 (NAB) 逆转了这些亲迁移和侵入性效应.
- 阿洛-阿卡治疗在体内减少了肺转移,减少了结节的数量和大小.
结论:
- 甲状腺癌细胞促进甲状腺癌细胞迁移和入侵通过通过外分勒提升MMP-2的调节.
- 莱普信号传递是ADSC驱动的甲状腺癌进展的关键调解者.
- 准勒素路径可能提供一种策略,以抵消与肥胖相关的甲状腺癌侵入性.
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