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神经胶质瘤会主动构建一个对自身有利的细胞外基质,以促进复发和进展。

Glioma actively orchestrate a self-advantageous extracellular matrix to promote recurrence and progression.

作者信息

Wei Ruolun, Zhou Jiasheng, Bui Brandon, Liu Xianzhi

机构信息

Department of Neurosurgery, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China.

Department of Neurosurgery, Stanford University, Stanford, CA, USA.

出版信息

BMC Cancer. 2024 Aug 8;24(1):974. doi: 10.1186/s12885-024-12751-3.

DOI:10.1186/s12885-024-12751-3
PMID:39118096
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11308147/
Abstract

The intricate interplay between cancer cells and their surrounding microenvironment has emerged as a critical factor driving the aggressive progression of various malignancies, including gliomas. Among the various components of this dynamic microenvironment, the extracellular matrix (ECM) holds particular significance. Gliomas, intrinsic brain tumors that originate from neuroglial progenitor cells, have the remarkable ability to actively reform the ECM, reshaping the structural and biochemical landscape to their advantage. This phenomenon underscores the adaptability and aggressiveness of gliomas, and highlights the intricate crosstalk between tumor cells and their surrounding matrix.In this review, we delve into how glioma actively regulates glioma ECM to organize a favorable microenvironment for its survival, invasion, progression and therapy resistance. By unraveling the intricacies of glioma-induced ECM remodeling, we gain valuable insights into potential therapeutic strategies aimed at disrupting this symbiotic relationship and curbing the relentless advance of gliomas within the brain.

摘要

癌细胞与其周围微环境之间复杂的相互作用已成为驱动包括神经胶质瘤在内的各种恶性肿瘤侵袭性进展的关键因素。在这个动态微环境的各种组成部分中,细胞外基质(ECM)具有特殊的重要性。神经胶质瘤是起源于神经胶质祖细胞的原发性脑肿瘤,具有积极重塑细胞外基质的显著能力,将结构和生化环境重塑为有利于自身的状态。这一现象凸显了神经胶质瘤的适应性和侵袭性,并突出了肿瘤细胞与其周围基质之间复杂的相互作用。在这篇综述中,我们深入探讨神经胶质瘤如何积极调节神经胶质瘤细胞外基质,以构建一个有利于其生存、侵袭、进展和治疗抵抗的微环境。通过揭示神经胶质瘤诱导的细胞外基质重塑的复杂性,我们获得了关于潜在治疗策略的宝贵见解,这些策略旨在破坏这种共生关系并遏制神经胶质瘤在脑内的持续发展。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/26d9/11308147/1863e2dd81df/12885_2024_12751_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/26d9/11308147/e9302fe5449b/12885_2024_12751_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/26d9/11308147/df6f28cc5a88/12885_2024_12751_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/26d9/11308147/1863e2dd81df/12885_2024_12751_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/26d9/11308147/e9302fe5449b/12885_2024_12751_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/26d9/11308147/df6f28cc5a88/12885_2024_12751_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/26d9/11308147/1863e2dd81df/12885_2024_12751_Fig3_HTML.jpg

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