CYP3A5 promotes glioblastoma stemness and chemoresistance through fine-tuning NAD+/NADH ratio

Journal of Experimental & Clinical Cancer Research, Journal Year: 2025, Volume and Issue: 44(1)

Published: Jan. 3, 2025

Language: Английский

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Mitochondrial DNA copy number alterations: Key players in the complexity of glioblastoma (Review)

Molecular Medicine Reports, Journal Year: 2025, Volume and Issue: 31(3)

Published: Jan. 24, 2025

Renowned as a highly invasive and lethal tumor derived from neural stem cells in the central nervous system, glioblastoma (GBM) exhibits substantial histopathological variation genomic complexity, which drive its rapid progression therapeutic resistance. Alterations mitochondrial DNA (mtDNA) copy number (CN) serve crucial role GBM development progression, affecting various aspects of biology, including energy production, oxidative stress regulation cellular adaptability. Fluctuations mtDNA levels, whether elevated or diminished, can impair function, potentially disrupting phosphorylation amplifying reactive oxygen species generation, thereby fueling growth influencing treatment responses. Understanding mechanisms mtDNA‑CN variations, their interplay with genetic environmental elements microenvironment, is essential for advancing diagnostic strategies. Targeting alterations could strengthen efficacy, mitigate resistance ultimately enhance prognosis patients this aggressive brain tumor. The present review summarizes existing literature on alterations, specifically emphasizing variations association by surveying articles published between 1996 2024, sourced databases such Scopus, PubMed Google Scholar. In addition, provides brief overview genome architecture, knowledge regarding integrity CN, how mitochondria significantly impact tumorigenesis. This further presents information approaches restoring that contribute to optimized function improved health outcomes.

Language: Английский

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Overcoming immunotherapy resistance in glioblastoma: challenges and emerging strategies

Frontiers in Pharmacology, Journal Year: 2025, Volume and Issue: 16

Published: March 28, 2025

Glioblastoma (GBM) is the most common and aggressive primary brain tumor in adults, characterized by rapid proliferation, extensive infiltration, significant intratumoral heterogeneity. Despite advancements conventional treatments, including surgery, radiotherapy, chemotherapy, prognosis for GBM patients remains poor, with a median survival of approximately 15 months. Immunotherapy has emerged as promising alternative; however, unique biological immunological features, its immunosuppressive microenvironment (TME) low mutational burden, render it resistant to many immunotherapeutic strategies. This review explores key challenges immunotherapy, focusing on immune evasion mechanisms, blood-brain barrier (BBB), TME. Immune checkpoint inhibitors CAR-T cells have shown promise preclinical models but limited clinical success due antigen heterogeneity, cell exhaustion, impaired trafficking across BBB. Emerging strategies, dual-targeting cells, engineered secreting therapeutic molecules, advanced delivery systems overcome BBB, show potential enhancing treatment efficacy. Addressing these crucial improving immunotherapy outcomes.

Language: Английский

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Deciphering novel mitochondrial signatures: multi-omics analysis uncovers cross-disease markers and oligodendrocyte pathways in Alzheimer’s disease and glioblastoma

Frontiers in Aging Neuroscience, Journal Year: 2025, Volume and Issue: 17

Published: Feb. 13, 2025

Introduction Alzheimer’s disease (AD) and glioblastoma (GBM) are severe neurological disorders that pose significant global healthcare challenges. Despite extensive research, the molecular mechanisms, particularly those involving mitochondrial dysfunction, remain poorly understood. A major limitation in current studies is lack of cell-specific markers effectively represent dynamics AD GBM. Methods In this study, we analyzed single-cell transcriptomic data using 10 machine learning algorithms to identify mitochondria-associated markers. We validated these through integration gene expression methylation across diverse cell types. Our dataset comprised single-nucleus RNA sequencing (snRNA-seq) from patients, (scRNA-seq) GBM additional DNA ROSMAP, ADNI, TCGA, CGGA cohorts. Results analysis identified four cross-disease markers: EFHD1, SASH1, FAM110B, SLC25A18 . These showed both shared unique profiles GBM, suggesting a common mechanism contributing diseases. Additionally, oligodendrocytes their interactions with astrocytes were implicated progression, APP signaling pathway. Key hub genes, such as HS6ST3 TUBB2B , different cellular subpopulations, highlighting co-expression network linked function.

Language: Английский

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Ferroptosis driven by nanoparticles for tackling glioblastoma

Cancer Letters, Journal Year: 2024, Volume and Issue: unknown, P. 217392 - 217392

Published: Dec. 1, 2024

Language: Английский

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