在循环的细胞外囊中增加的细胞外基因蛋白1在肥胖条件下支持乳腺癌的进展
Keyang Xu1, Ai Fu2, Zhaoyi Li2
1Centre for Cancer & Inflammation Research, School of Chinese Medicine, Hong Kong Baptist University, Hong Kong, China.
Nature communications
|February 24, 2024
概括
肥胖会增加小细胞外囊泡 (sEVs) 中的细胞外基质蛋白1 (ECM1),促进乳腺癌 (BC) 的生长和转移. 针对这种ECM1-sEV通路为与肥胖相关的BC.提供了新的治疗策略.
科学领域:
- 生物化学 生物化学
- 细胞生物学 细胞生物学
- 在瘤学瘤学.
背景情况:
- 小细胞外囊泡 (sEVs) 的载荷在疾病中发生变化.
- 细胞外矩阵蛋白1 (ECM1) 在乳腺癌 (BC) 进展中的作用.
研究的目的:
- 研究肥胖症中通过sEVs传输ECM1及其对BC的影响.
- 阐明ECM1介导的BC转移的机制.
主要方法:
- 利用肥胖和乳腺癌的小鼠模型.
- 分析了循环中的SEV和细胞中的蛋白质水平.
- 研究了整合蛋白-β2在ECM1运输中的作用.
- 在体外和体内评估了饮食诱导的肥胖sEVs (D-sEVs) 对BC细胞的影响.
主要成果:
- 肥胖症在循环中的sEV中显著提高ECM1蛋白,依赖于整合素-β2.2.
- 由D-sEVs传递的ECM1增强了BC细胞的入侵,迁移和转移.
- 在BC细胞中ECM1升高会增加MMP3和S100A/B水平,促进瘤生长.
结论:
- 在肥胖期间,整体蛋白-β2调解了SEV中的ECM1丰富.
- 由肥胖引起的sEVs通过ECM1传递促进BC的进展.
- 准ECM1-sEV轴为与肥胖相关的BC.提供了潜在的治疗策略.
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