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向瘤关联细胞中的TCF21-TCF3异构体,通过恢复细胞守门员功能来减轻血液转移
Wenqian Yin1, Haiqin Yao2, Xiaobo Li1
1State Key Laboratory of Bioactive Molecules and Druggability Assessment, Guangdong Basic Research Center of Excellence for Natural Bioactive Molecules and Discovery of Innovative Drugs, Jinan University, Guangzhou 510632, China; College of Pharmacy, Jinan University, Guangzhou 510632, China; Guangdong-Hong Kong-Macau Joint Laboratory for Pharmacodynamic Constituents of TCM and New Drugs Research, Guangdong Province Key Laboratory of Pharmacodynamic Constituents of TCM and New Drugs Research, Jinan University, Guangzhou 510632, Guangdong, China.
研究人员在瘤周细胞中发现了一种TCF21-TCF3转录因子,该因子驱动癌症转移. 一种针对这种相互作用的新可以通过恢复细胞周围细胞功能,在临床前模型中显著抑制转移.
科学领域:
- 在瘤学瘤学.
- 分子生物学分子生物学
- 生物化学 生物化学
背景情况:
- 血液转移是癌症死亡的主要原因.
- 瘤周围细胞功能障碍对于促进癌症扩散至关重要.
- 目前的抗细胞疗法可能会悖论地增强转移.
研究的目的:
- 确定驱动转移的TPC特有的分子机制.
- 制定一个有针对性的治疗策略,以抑制TPC介导的转移.
- 研究TCF21-TCF3异构体在癌症进展中的作用.
主要方法:
- 确定了TCF21-TCF3作为瘤周细胞中的关键转录因子异构体.
- 设计了一种抑制剂,针对TCF21-TCF3相互作用.
- 在大肠直肠癌和骨肉瘤的小鼠模型中评估了的疗效.
主要成果:
- TCF21-TCF3通过原氧化和ECM沉积驱动转移.
- 设计的干扰了TCF21-TCF3的二分化.
- 类治疗显著抑制了转移,并在体内恢复了细胞周围细胞守门员的功能.
结论:
- TCF21-TCF3是一种新的治疗点,用于预防癌症转移.
- 一个由TCF21衍生的提供了一种有希望的策略来抑制TPC驱动的转移.
- 恢复细胞周细胞功能是抑制转移性传播的关键.
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