癌细胞可塑性的新兴范式
Hyunbin D Huh1, Hyun Woo Park1
1Department of Biochemistry, Brain Korea 21 Project, College of Life Science and Biotechnology, Yonsei University, Seoul 03722, Korea.
BMB reports
|April 17, 2024
概括
癌细胞通过表皮转移到介质细胞转移 (EMT) 和附着转移到悬浮转移 (AST) 适应转移. 了解这些细胞可塑性机制是开发新癌症疗法的关键.
科学领域:
- 在瘤学瘤学.
- 细胞生物学 细胞生物学
- 分子生物学分子生物学
背景情况:
- 癌细胞在瘤微环境 (TME) 中适应,以促进转移.
- 细胞可塑性,包括上皮转移到介质细胞 (EMT) 和附着转移到悬浮 (AST),使癌细胞能够入侵和扩散.
- 通过组织活检识别的EMT涉及转录因子 (TFs),促进介质细胞特征的迁移.
- 通过液体活检识别的AST涉及AST-TFs重新编程用于循环瘤细胞 (CTC) 传播的 anchorage依赖性.
研究的目的:
- 审查在转移级联期间控制AST和EMT细胞可塑性的机制.
- 讨论EMT和AST所带来的治疗挑战.
- 为开发针对癌症转移的新型治疗干预措施提供见解.
主要方法:
- 关于表皮细胞转化为介质细胞转化 (EMT) 的研究的文献综述.
- 关于粘附到悬浮过渡 (AST) 研究的文献综述.
- 对驱动癌症转移中的细胞可塑性的机制的分析.
- 讨论针对EMT和AST的治疗策略.
主要成果:
- EMT和AST是关键的细胞适应,使癌细胞入侵,传播和殖民成为可能.
- 这些转变在转移过程中动态地改变了细胞-细胞和细胞-矩阵相互作用.
- 了解EMT和AST的可塑性对于向转移性过程至关重要.
结论:
- EMT和AST代表细胞可塑性驱动癌症转移的关键机制.
- 针对与EMT和AST相关的可塑性提出了治疗挑战,但也为干预提供了机会.
- 对这些转变的进一步研究可以为开发更有效的抗转移疗法提供信息.
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