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非编码 RNA 在胶质母细胞瘤发生中表观遗传失调中的作用。

The Role of Non-Coding RNAs in Epigenetic Dysregulation in Glioblastoma Development.

机构信息

Research Center for Functional Genomics, Biomedicine and Translational Medicine, Iuliu Hatieganu University of Medicine and Pharmacy, 400337 Cluj-Napoca, Romania.

Department of Microbiology, Oslo University Hospital, 0424 Oslo, Norway.

出版信息

Int J Mol Sci. 2023 Nov 14;24(22):16320. doi: 10.3390/ijms242216320.


DOI:10.3390/ijms242216320
PMID:38003512
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10671451/
Abstract

Glioblastoma (GBM) is a primary brain tumor arising from glial cells. The tumor is highly aggressive, the reason for which it has become the deadliest brain tumor type with the poorest prognosis. Like other cancers, it compromises molecular alteration on genetic and epigenetic levels. Epigenetics refers to changes in gene expression or cellular phenotype without the occurrence of any genetic mutations or DNA sequence alterations in the driver tumor-related genes. These epigenetic changes are reversible, making them convenient targets in cancer therapy. Therefore, we aim to review critical epigenetic dysregulation processes in glioblastoma. We will highlight the significant affected tumor-related pathways and their outcomes, such as regulation of cell cycle progression, cell growth, apoptosis, angiogenesis, cell invasiveness, immune evasion, or acquirement of drug resistance. Examples of molecular changes induced by epigenetic modifications, such as DNA epigenetic alterations, histone post-translational modifications (PTMs), and non-coding RNA (ncRNA) regulation, are highlighted. As understanding the role of epigenetic regulators and underlying molecular mechanisms in the overall pro-tumorigenic landscape of glioblastoma is essential, this literature study will provide valuable insights for establishing the prognostic or diagnostic value of various non-coding transcripts, including miRNAs.

摘要

胶质母细胞瘤(GBM)是一种起源于神经胶质细胞的原发性脑肿瘤。这种肿瘤具有高度侵袭性,是导致其成为最致命的脑肿瘤类型和预后最差的原因。与其他癌症一样,它在遗传和表观遗传层面上存在分子改变。表观遗传学是指在不发生驱动肿瘤相关基因的任何基因突变或 DNA 序列改变的情况下,基因表达或细胞表型的变化。这些表观遗传变化是可逆的,使其成为癌症治疗的便利靶点。因此,我们旨在综述胶质母细胞瘤中关键的表观遗传失调过程。我们将重点介绍受影响的重要肿瘤相关途径及其结果,如细胞周期进程、细胞生长、细胞凋亡、血管生成、细胞侵袭、免疫逃逸或获得耐药性的调节。还强调了由表观遗传修饰诱导的分子变化的例子,如 DNA 表观遗传改变、组蛋白翻译后修饰(PTMs)和非编码 RNA(ncRNA)的调节。由于了解表观遗传调节剂在胶质母细胞瘤整体促肿瘤发生景观中的作用及其潜在的分子机制至关重要,因此这项文献研究将为确定各种非编码转录物(包括 miRNA)的预后或诊断价值提供有价值的见解。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5346/10671451/bd0e46c64c75/ijms-24-16320-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5346/10671451/bd0e46c64c75/ijms-24-16320-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5346/10671451/bd0e46c64c75/ijms-24-16320-g001.jpg

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[1]
The Role of Non-Coding RNAs in Epigenetic Dysregulation in Glioblastoma Development.

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[2]
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[3]
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[10]
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引用本文的文献

[1]
Advanced nanotheranostic approaches for targeted glioblastoma treatment: a synergistic fusion of CRISPR-Cas gene editing, AI-driven tumor profiling, and BBB-modulation.

Med Oncol. 2025-8-7

[2]
Epitranscriptomic alterations induced by environmental toxins: implications for RNA modifications and disease.

Genes Environ. 2025-8-4

[3]
Androgen receptor inhibition sensitizes glioblastoma stem cells to temozolomide by the miR-1/miR-26a-1/miR-487b signature mediated WT1 and FOXA1 silencing.

Cell Death Discov. 2025-5-21

[4]
Identification of distinct profiles of glioblastoma through the immunocapture of extracellular vesicles from patient plasma.

PLoS One. 2025-3-19

[5]
Triple‑negative breast cancer cell‑derived piR‑31115 promotes the proliferation and migration of endothelial cells via METTL3‑mediated m6A modification of YAP1.

Oncol Rep. 2025-3

[6]
Ubiquitination of p21 by E3 ligase RNF135 promotes the proliferation of human glioblastoma cells.

Oncol Lett. 2024-6-27

[7]
CRISPR/Cas9-Mediated Gene Therapy for Glioblastoma: A Scoping Review.

Biomedicines. 2024-1-21

本文引用的文献

[1]
Next-generation bromodomain inhibitors of the SWI/SNF complex enhance DNA damage and cell death in glioblastoma.

J Cell Mol Med. 2023-9

[2]
Clinical Theranostics Trademark of Exosome in Glioblastoma Metastasis.

ACS Biomater Sci Eng. 2023-9-11

[3]
The role of chromatin remodeler SMARCA4/BRG1 in brain cancers: a potential therapeutic target.

Oncogene. 2023-7

[4]
Crosstalk between miRNAs and DNA Methylation in Cancer.

Genes (Basel). 2023-5-12

[5]
The function of histone methylation and acetylation regulators in GBM pathophysiology.

Front Oncol. 2023-5-2

[6]
New perspective on DNA response pathway (DDR) in glioblastoma, focus on classic biomarkers and emerging roles of ncRNAs.

Expert Rev Mol Med. 2023-5-8

[7]
HDAC1 mediates epithelial-mesenchymal transition and promotes cancer cell invasion in glioblastoma.

Pathol Res Pract. 2023-6

[8]
Proteomic analysis reveals microvesicles containing NAMPT as mediators of radioresistance in glioma.

Life Sci Alliance. 2023-6

[9]
MiR-10b-5p Impairs TET2-Mediated Inhibition of PD-L1 Transcription Thus Promoting Immune Evasion and Tumor Progression in Glioblastoma.

Tohoku J Exp Med. 2023-7-8

[10]
Molecular Pathways Implicated in Radioresistance of Glioblastoma Multiforme: What Is the Role of Extracellular Vesicles?

Int J Mol Sci. 2023-3-2

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