Inflammatory Mediators and GBM Malignancy: Current Scenario and Future Prospective DOI Open Access
Ilya V. Ulasov,

Vaishali Singh,

Anastasia Laevskaya

et al.

Discovery Medicine, Journal Year: 2023, Volume and Issue: 35(177), P. 458 - 458

Published: Jan. 1, 2023

Glioblastoma multiforme is one of the most widespread and dangerous forms brain tumor with high inflammation. The microenvironment comprises diverse cells, different types immune extracellular matrix. Inflammatory mediators like chemokines, cytokines, growth factors possibly serve as a capable therapeutic target to quash their tumor-promoting properties in glioblastoma (GBM). Cytokines are heterogeneous group soluble functional proteins which also associated induction progression tumors. These supposed have both pro-inflammatory (such necrosis factor-α (TNF-α), interleukin-17A (IL-17A), interferon-γ (IFN-γ), IL-4, IL-2, IL-6, IL-12, IL-13) anti-inflammatory transforming factor-β (TGF-β), IL-10, granulocyte-macrophage colony-stimulating factor (GM-CSF)) actions crucial communications channels microenvironment. In present minireview we discuss inflammatory focus on involvement cytokines establishing communication presented data highlight possible roles between cells formed by protect host organs while secreted used for advantage. Though clinical trials number immunotherapeutic agents going around globe, there still requirement thorough investigation regulatory mechanism managing GBM growth, recurrence, response therapy.

Language: Английский

Epigenetic regulation of tumor-immune symbiosis in glioma DOI Creative Commons
Yang Liu, Heba Ali, Fatima Khan

et al.

Trends in Molecular Medicine, Journal Year: 2024, Volume and Issue: 30(5), P. 429 - 442

Published: March 7, 2024

Glioma is a type of aggressive and incurable brain tumor. Patients with glioma are highly resistant to all types therapies, including immunotherapies. Epigenetic reprogramming key molecular hallmark in tumors across cancer types, glioma. Mounting evidence highlights pivotal role epigenetic regulation shaping tumor biology therapeutic responses through mechanisms involving both cells immune cells, as well their symbiotic interactions the microenvironment (TME). In this review, we discuss that impacts cell immunity cell-autonomous non-cell-autonomous manner. Moreover, provide an overview potential approaches can disrupt epigenetic-regulated tumor-immune symbiosis TME.

Language: Английский

Citations

6

Expanding Role of Epigenetics in Human Health and Disease DOI Open Access
Swarup K. Chakrabarti, Dhrubajyoti Chattopadhyay

Exploratory Research and Hypothesis in Medicine, Journal Year: 2024, Volume and Issue: 000(000), P. 000 - 000

Published: Jan. 11, 2024

The traditional definition of epigenetics encompasses all molecular pathways that affect how a genotype expresses itself on the way to particular phenotype, with serving as interface between and phenotype. Unlike genetic changes, which may have protracted, irreversible effects health emergence illnesses, epigenetic modifications are reversible do not change DNA sequence. However, they can our bodies interpret sequences. Gene expression regulated by has emerged major contributing element etiology many diseases over time crucial determinant human health. One strongest arguments in support gene controlled comes from startling discovery methylation causes X-chromosome inactivation, been connected several diseases. intrinsic uterine environment, where embryo fetus grow develop become neonates is vulnerable early settings throughout development, affecting offspring's long-term well their predisposition for different germ cell development influenced environmental factors, result transgenerational effects. Therefore, this article, we essentially provide summary present level understanding concerning function regarding critical facets health, including embryonic adulthood, emphasis explaining underlying diverse mechanisms regulate onset diseases, cutting-edge technological tools used study epigenome. Finally, talk about state therapies, might be put use treatment range

Language: Английский

Citations

5

Natural products modulating epigenetic mechanisms by affecting histone methylation/demethylation: Targeting cancer cells DOI
Dawid Dorna, Adriana Grabowska, Jarosław Paluszczak

et al.

British Journal of Pharmacology, Journal Year: 2023, Volume and Issue: unknown

Published: Sept. 13, 2023

Many natural products can exert anticancer or chemopreventive activity by interfering with the cellular epigenetic machinery. studies indicate relevance of affecting DNA methylation and histone acetylation, however influence on mechanisms related to are often overlooked. This may be associated lagging evidence that changes in action writers erasers, subsequent alterations profile causally carcinogenesis. Recent animal have shown targeting methylation/demethylation affects course experimentally induced Existing data suggest numerous compounds from different chemical groups, including green tea polyphenols other flavonoids, curcuminoids, stilbene derivatives, phenolic acids, isothiocyanates, alkaloids terpenes, affect expression crucial enzymes involved demethylation lysine arginine residues. These activities been modulation cancer-related gene functional changes, reduced cell proliferation migration, enhanced apoptosis various cancer models. Most focused and/or two proteins - EZH2 (a H3K27 methyltransferase) LSD1 (lysine demethylase 1A a H3K4/9 demethylase), effects global levels caused phytochemicals, but regarding methyltransferases demethylases scarce. While field remains relatively unexplored, this review aims explore impact methylation/demethylation, showing their carcinogenesis progression.

Language: Английский

Citations

11

The epigenetic mechanisms involved in the treatment resistance of glioblastoma DOI Open Access

Aanya Shahani,

Hasan Slika, Ahmed Elbeltagy

et al.

Cancer Drug Resistance, Journal Year: 2025, Volume and Issue: unknown

Published: Feb. 25, 2025

Glioblastoma (GBM) is an aggressive malignant brain tumor with almost inevitable recurrence despite multimodal management surgical resection and radio-chemotherapy. While several genetic, proteomic, cellular, anatomic factors interplay to drive promote treatment resistance, the epigenetic component remains among most versatile heterogeneous of these factors. Herein, landscape GBM refers a myriad modifications processes that can alter gene expression without altering genetic code cancer cells. These encompass DNA methylation, histone modification, chromatin remodeling, non-coding RNA molecules, all which have been found be implicated in augmenting tumor’s behavior driving its resistance therapeutics. This review aims delve into underlying interactions mediate this role for each components. Further, it discusses two-way relationship between heterogeneity plasticity, are crucial effectively treat GBM. Finally, we build on previous characterization explore specific targets investigated development promising therapeutic agents.

Language: Английский

Citations

0

The Spectrum of Molecular Pathways in Gliomas—An Up-to-Date Review DOI Creative Commons
Reinhold Nafe, Elke Hattingen

Biomedicines, Journal Year: 2023, Volume and Issue: 11(8), P. 2281 - 2281

Published: Aug. 16, 2023

During the last 20 years, molecular alterations have gained increasing significance in diagnosis and biological assessment of tumors. Gliomas represent largest group tumors central nervous system, main aim this review is to present current knowledge on pathways their gliomas. A wide range new insights has been gained, including evidence for involvement WNT pathway or hippo pathobiology gliomas, indicating a broad different formerly not considered play role Even aspects angiogenic, apoptotic, metabolic are presented, as well rapidly growing field epigenetic processes, non-coding RNAs. The two major conclusions drawn from distinct interconnectivity whole spectrum prominent RNAs, especially circular regulation specific targets. All these discussed, even considering topic resistance therapy along with that still incompletely understood, like hydroxymethylation, ferroptosis,

Language: Английский

Citations

10

Uracil‐ and Pyridine‐Containing HDAC Inhibitors Displayed Cytotoxicity in Colorectal and Glioblastoma Cancer Stem Cells DOI
Francesco Fiorentino, Emanuele Fabbrizi, A. Russo Raucci

et al.

ChemMedChem, Journal Year: 2024, Volume and Issue: 19(13)

Published: March 26, 2024

Abstract Cancer stem cells (CSCs) are a niche of highly tumorigenic featuring self‐renewal, activation pluripotency genes, multidrug resistance, and ability to cause cancer relapse. Seven HDACi ( 1 ‐ 7 ), showing either hydroxamate or 2′‐aminoanilide function, were tested in colorectal (CRC) glioblastoma multiforme (GBM) CSCs determine their effects on cell proliferation, H3 acetylation levels in‐cell HDAC activity. Two uracil‐based hydroxamates, 5 6 , which differ substitution at C5 C6 positions the pyrimidine ring, exhibited greatest cytotoxicity GBM ) CRC CSCs, followed by pyridine‐hydroxamate 2 with 2‐ 6‐fold higher potency than positive control SAHA. Finally, increased as well inhibition directly selected 4 confirmed target engagement. Further investigation will be conducted into broad‐spectrum anticancer properties most potent derivatives combination approved, conventional drugs.

Language: Английский

Citations

3

The Role of Non-Coding RNAs in Epigenetic Dysregulation in Glioblastoma Development DOI Open Access
Ekaterina Isachesku, Cornelia Braicu, Radu Pîrlog

et al.

International Journal of Molecular Sciences, Journal Year: 2023, Volume and Issue: 24(22), P. 16320 - 16320

Published: Nov. 14, 2023

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

Language: Английский

Citations

6

Identification and characterization of putative biomarkers and therapeutic axis in Glioblastoma multiforme microenvironment DOI Creative Commons
Smita Kumari, Pravir Kumar

Frontiers in Cell and Developmental Biology, Journal Year: 2023, Volume and Issue: 11

Published: July 19, 2023

Non-cellular secretory components, including chemokines, cytokines, and growth factors in the tumor microenvironment, are often dysregulated, impacting tumorigenesis Glioblastoma multiforme (GBM) where prognostic significance of current treatment remains unsatisfactory. Recent studies have demonstrated potential post-translational modifications (PTM) their respective enzymes, such as acetylation ubiquitination GBM etiology through modulating signaling events. However, relationship between non-cellular components will create a research void therapeutics. Therefore, we aim to bridge gap PTM machine learning computational biology approaches. Herein, highlighted importance BMP1, CTSB, LOX, LOXL1, PLOD1, MMP9, SERPINE1, SERPING1 etiology. Further, positive E2 conjugating enzymes (Ube2E1, Ube2H, Ube2J2, Ube2C, Ube2S), E3 ligases (VHL GNB2L1) substrate (HIF1A). Additionally, reported novel HAT1-induced sites Ube2S (K211) Ube2H (K8, K52). Structural functional characterization (8) (1) identified association with protein kinases. Lastly, our results found putative therapeutic axis HAT1-Ube2S(K211)-GNB2L1-HIF1A predictive biomarkers (CTSB, HAT1, VHL, that play critical role pathogenesis.

Language: Английский

Citations

4

ADCY5 act as a putative tumor suppressor in glioblastoma: An integrated analysis DOI Creative Commons
Can Wang,

Wen Yan,

Huang Luo

et al.

Heliyon, Journal Year: 2024, Volume and Issue: 10(17), P. e37012 - e37012

Published: Aug. 27, 2024

Language: Английский

Citations

1

Inflammatory Mediators and GBM Malignancy: Current Scenario and Future Prospective DOI Open Access
Ilya V. Ulasov,

Vaishali Singh,

Anastasia Laevskaya

et al.

Discovery Medicine, Journal Year: 2023, Volume and Issue: 35(177), P. 458 - 458

Published: Jan. 1, 2023

Glioblastoma multiforme is one of the most widespread and dangerous forms brain tumor with high inflammation. The microenvironment comprises diverse cells, different types immune extracellular matrix. Inflammatory mediators like chemokines, cytokines, growth factors possibly serve as a capable therapeutic target to quash their tumor-promoting properties in glioblastoma (GBM). Cytokines are heterogeneous group soluble functional proteins which also associated induction progression tumors. These supposed have both pro-inflammatory (such necrosis factor-α (TNF-α), interleukin-17A (IL-17A), interferon-γ (IFN-γ), IL-4, IL-2, IL-6, IL-12, IL-13) anti-inflammatory transforming factor-β (TGF-β), IL-10, granulocyte-macrophage colony-stimulating factor (GM-CSF)) actions crucial communications channels microenvironment. In present minireview we discuss inflammatory focus on involvement cytokines establishing communication presented data highlight possible roles between cells formed by protect host organs while secreted used for advantage. Though clinical trials number immunotherapeutic agents going around globe, there still requirement thorough investigation regulatory mechanism managing GBM growth, recurrence, response therapy.

Language: Английский

Citations

3