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胶质母细胞瘤细胞中推测的间充质刺激的转录组特征差异。

Divergent transcriptomic signatures from putative mesenchymal stimuli in glioblastoma cells.

机构信息

Department of Chemical Engineering, University of Virginia, Charlottesville, VA, 22903, USA.

Department of Neurology, University of Virginia, Charlottesville, VA, 22903, USA.

出版信息

Cancer Gene Ther. 2024 Jun;31(6):851-860. doi: 10.1038/s41417-023-00724-w. Epub 2024 Feb 9.

DOI:10.1038/s41417-023-00724-w
PMID:38337036
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11192628/
Abstract

In glioblastoma, a mesenchymal phenotype is associated with especially poor patient outcomes. Various glioblastoma microenvironmental factors and therapeutic interventions are purported drivers of the mesenchymal transition, but the degree to which these cues promote the same mesenchymal transitions and the uniformity of those transitions, as defined by molecular subtyping systems, is unknown. Here, we investigate this question by analyzing publicly available patient data, surveying commonly measured transcripts for mesenchymal transitions in glioma-initiating cells (GIC), and performing next-generation RNA sequencing of GICs. Analysis of patient tumor data reveals that TGFβ, TNFα, and hypoxia signaling correlate with the mesenchymal subtype more than the proneural subtype. In cultured GICs, the microenvironment-relevant growth factors TGFβ and TNFα and the chemotherapeutic temozolomide promote expression of commonly measured mesenchymal transcripts. However, next-generation RNA sequencing reveals that growth factors and temozolomide broadly promote expression of both mesenchymal and proneural transcripts, in some cases with equal frequency. These results suggest that glioblastoma mesenchymal transitions do not occur as distinctly as in epithelial-derived cancers, at least as determined using common subtyping ontologies and measuring response to growth factors or chemotherapeutics. Further understanding of these issues may identify improved methods for pharmacologically targeting the mesenchymal phenotype in glioblastoma.

摘要

在胶质母细胞瘤中,间充质表型与患者预后特别差有关。各种胶质母细胞瘤微环境因素和治疗干预被认为是间充质转化的驱动因素,但这些线索在多大程度上促进相同的间充质转化,以及这些转化的一致性,如分子亚型系统所定义的,尚不清楚。在这里,我们通过分析公开可用的患者数据、调查神经胶质瘤起始细胞(GIC)中常见的间充质转化测量转录本以及对 GIC 进行下一代 RNA 测序来研究这个问题。对患者肿瘤数据的分析表明,TGFβ、TNFα 和缺氧信号与间充质亚型的相关性强于神经前体亚型。在培养的 GIC 中,与微环境相关的生长因子 TGFβ 和 TNFα 以及化疗药物替莫唑胺促进了常见测量的间充质转录本的表达。然而,下一代 RNA 测序显示,生长因子和替莫唑胺广泛促进了间充质和神经前体转录本的表达,在某些情况下频率相同。这些结果表明,胶质母细胞瘤的间充质转化并不像上皮源性癌症那样明显,至少使用常见的分型本体和测量对生长因子或化疗药物的反应来确定是这样。进一步了解这些问题可能会确定出改善的方法,以药理学靶向胶质母细胞瘤中的间充质表型。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e40/11192628/c0ab64af0a02/41417_2023_724_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e40/11192628/df32b2d2a383/41417_2023_724_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e40/11192628/70cd2ace9a26/41417_2023_724_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e40/11192628/b9423b24bde8/41417_2023_724_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e40/11192628/75cabac665e1/41417_2023_724_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e40/11192628/c0ab64af0a02/41417_2023_724_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e40/11192628/df32b2d2a383/41417_2023_724_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e40/11192628/70cd2ace9a26/41417_2023_724_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e40/11192628/b9423b24bde8/41417_2023_724_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e40/11192628/75cabac665e1/41417_2023_724_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e40/11192628/c0ab64af0a02/41417_2023_724_Fig5_HTML.jpg

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