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通过细胞外基质蛋白1a重塑瘤微环境,可以差异调节卵巢癌转移的发生
Yinjue Yu1, Cuiting Lyu2, Xiaojing Li3
1Central Laboratory, The Fifth People's Hospital of Shanghai, Fudan University, Shanghai, 200140, China; Department of Radiotherapy, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, 200127, China.
Cancer letters
|June 7, 2024
概括
细胞外矩阵蛋白1异型a (ECM1a) 在上皮卵巢癌 (EOC) 转移中具有双重作用. 它通过将干细胞转化为与癌症相关的纤维细胞来促进瘤进展和远程转移,但抑制了早期腹转移.
科学领域:
- 在瘤学瘤学.
- 癌症生物学 癌症生物学
- 瘤微环境研究 研究
背景情况:
- 细胞外矩阵蛋白1异型a (ECM1a) 之前已经被证明可以通过自身隐性信号传递促进上皮卵巢癌 (EOC).
- 瘤微环境 (TME) 中ECM1a作为分泌分子的功能尚不清楚.
- 了解ECM1a的作用对于破译EOC进展和转移至关重要.
研究的目的:
- 研究ECM1a在瘤微环境中的EOC转移中的双重功能.
- 阐明ECM1a影响癌症相关纤维细胞 (CAF) 分化和细胞外基质 (ECM) 重塑的机制.
- 探索ECM1a,骨髓介质干细胞 (BMSC) 和血管类蛋白2 (ANGPTL2) 在EOC进展中的相互作用.
主要方法:
- 构建小鼠ECM1a-knockin和人类ECM1a-knockin小鼠模型.
- 生成 орто托普和腹腔外移植瘤模型,以模拟EOC转移.
- 分析ECM重建,BMSC招聘和差异化以及CAF转型.
主要成果:
- ECM1a 证明了双重作用,在 ортотоп模型中诱导转移,同时抑制早期腹膜转移.
- ECM1a通过招募和转化BMSCs到血小板衍生生长因子受体β (PDGFRβ+) CAFs来促进远程转移.
- ECM1a促进ANGPTL2分泌,它也与整合素αX相互作用,并影响BMSC分化.
结论:
- 在EOC进展和转移中,ECM1a表现出上下文依赖的双重功能.
- 通过影响BMSC分化为CAF和调节ECM组成,ECM1a显著重塑了TME.
- 这项研究强调了EOC表型异质性和转移潜力的复杂性,受ECM1a在TME内的复杂相互作用的影响.
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