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在神经母细胞瘤瘤微环境中,miR-574-5p的多重功能

Eva Proestler¹, Julia Donzelli¹, Sheila Nevermann¹

¹Fachbereich Biologie, Technische Universität Darmstadt, Darmstadt, Germany.

Frontiers in pharmacology

|September 21, 2023

概括

微RNAmiR-574-5p和前列腺素E2 (PGE2) 在神经母细胞瘤瘤微环境中相互作用. 这种相互作用会影响细胞外囊泡的通信,影响纤维细胞分化和瘤进展.

科学领域:

在瘤学瘤学.
分子生物学分子生物学
细胞生物学细胞生物学

背景情况:

神经母细胞瘤是一种常见的儿童癌症,涉及瘤微环境 (TME).
前列腺素E2 (PGE2) 是一种关键的炎症调解剂,促进神经母细胞瘤的进展.
通过细胞外囊泡 (EVs) 的细胞间通信在TME中发挥着关键作用.

研究的目的:

研究微RNAmiR-574-5p的作用及其与神经母细胞瘤中CUG结合蛋白1 (CUGBP1) 的相互作用.
阐明PGE2生物合成的机制及其在神经母细胞细胞内的miR-574-5p调节.
确定miR-574-5p通过神经母细胞瘤TME中小细胞外囊泡 (sEVs) 运输的功能.

主要方法:

研究了miR-574-5p和CUGBP1之间的相互作用,以诱导微粒体前列腺素E2合成酶1 (mPGES-1) 的表达.
分析了PGE2对miR-574-5p被分类成SEVs的影响.
研究了sEV衍生的miR-574-5p在纤维细胞上的膜功能,包括Toll-like受体7/8 (TLR7/8) 激活和α-平滑肌肉活性蛋白 (α-SMA) 表达.
在神经母细胞瘤中比较sEV衍生的miR-574-5p的功能与其在肺癌中的功能.

主要成果:

miR-574-5p和CUGBP1的相互作用诱导mPGES-1,导致神经母细胞瘤中PGE2生物合成的增加.
PGE2促进了miR-574-5p的包装到sEV中进行细胞间通信.
由sEV衍生的miR-574-5p作为TLR7/8的配体,通过α-SMA表达诱导纤维细胞分化.
在肺癌中表现出sEV衍生的miR-574-5p的相反的自身分泌功能,抑制PGE2生物合成.

结论:

在神经母细胞瘤中,miR-574-5p/CUGBP1轴调节PGE2的产生.
将miR-574-5p由PGE2介导分类为sEV是一种用于细胞间通信的新机制.
来自sEV的miR-574-5p在不同类型的瘤中具有不同的作用,突出显示了环境依赖的功能.
在sEV上的拉斯巴宁成分可能会影响运输的microRNAs的功能结果.

关键词:

在NSCLCLC中,我们可以看到.在PGE2的基础上,PGE2 在TLR7/8/8上.在 miR-574-5p 中.神经母细胞瘤的神经母细胞瘤它们包括四西班牙素.

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