Skip to content
DraconiticResearch
Search Sources API
203,234 studies31 sourcesUpdated 43 min ago
Peer-reviewedCC BYFrontiers in oncology

Targeting NOTCH-immune crosstalk in gliomas: from mechanisms to therapeutics.

  • Safieh Ebrahimi1,2,3
  • NoorMohammad Meshkinkhood2
  • Ali Aliee4
  • Li Yuhan5
  • Maryam Koulivand2
  • Zahra Koulivand2
  • Ali Gorji6,7
7 affiliations
  1. 1Bioinformatics Research Center, Basic Sciences Research Institute, Mashhad University of Medical Sciences, Mashhad, Iran.
  2. 2Shefa Neuroscience Research Center, Khatam Alanbia Hospital, Tehran, Iran.
  3. 3Department of Clinical Biochemistry, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran.
  4. 4Department of Clinical Biochemistry, Kermanshah University of Medical Sciences, Kermanshah, Iran.
  5. 5Department of Neurosurgery, Xinhua Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China.
  6. 6Epilepsy Research Center, Department of Neurosurgery, Münster University, Münster, Germany.
  7. 7Neuroscience Research Center, Mashhad University of Medical Sciences, Mashhad, Iran.
Read full textPDFDOICite

Abstract

Glioblastoma (GBM) is a highly aggressive and treatment-resistant malignancy characterized by an immunosuppressive tumor microenvironment (TME) that promotes disease progression and poor clinical outcomes. Increasing evidence suggests that NOTCH signaling is a key regulator of GBM progression, governing both tumor cell plasticity and immune evasion. In addition to its roles in development and stem cell maintenance, NOTCH signaling modulates interactions among glioma stem-like cells, immune cells, and stromal components. NOTCH signaling in both tumor and stromal compartments modulates immune cell fate decisions, antigen presentation, and inflammatory cytokine expression. This suggests its potential role as a key modulator of immune crosstalk within the TME of GBM. Moreover, dysregulation of the NOTCH signaling pathway may lead to an immunosuppressive TME, enhance tumor heterogeneity, and restrict responses to conventional therapies. Recent investigations also reveal the epigenetic and non-coding RNA patterns that reinforce aberrant NOTCH activity in GBM. Understanding the multifaceted interactions among NOTCH signaling, oncogenic pathways, and immunomodulatory mechanisms could provide insights into the molecular pathogenesis of GBM progression. Here, we discuss the pleiotropic and context-dependent functions of NOTCH signaling in GBM, with particular emphasis on its implications for tumor-immune interactions and its potential as a therapeutic target to address immune escape and treatment resistance.

Related

  1. Inflammation–fibrosis crosstalk in endometriosis: immune–stromal mechanisms linking lesion persistence to pain and infertility
    Xiaofeng Liu, Zheng Qu, Jinhong Gu +2
    Frontiers in medicinePeer-reviewedCC BYFull textGeneral medicineEurope PMC
  2. Microbiome-Immune Crosstalk in Inflammatory Skin Diseases: Mechanisms and Therapeutic Potential of Probiotics.
    Pranvi Sharma, Tanaka Nhokwara, Jaswinder Singh +2
    Immunity, inflammation and diseasePeer-reviewedCC BYFull textGeneral medicineEurope PMCPMC
  3. Glioblastoma stem cell–immune microenvironment crosstalk: molecular mechanisms and therapeutic opportunities
    Chuanhai Xu, Linlin Chai, Wei Yuan
    Frontiers in ImmunologyPeer-reviewedCC BY 4.0Full textHuman geneticsCrossrefEurope PMC
  4. Th17 cells and neutrophils: exploiting their crosstalk for multiple sclerosis therapeutics
    Jacob V Martin, Caleb Wong Han, Anne Brüstle +1
    Journal of NeuroinflammationPeer-reviewedCC BY-NC-ND 4.0Full textNeurologyPMC
  5. Cancer Outcomes in Cardiovascular Trials of Inflammation-Targeting Therapeutics
    Laura I. Yousif, Wouter C. Meijers, Rudolf A. de Boer
    JACC: CardioOncologyPeer-reviewedCC BY-NC-ND 4.0Full textOncologyPMC

Cite

BibTeXRIS
BibTeX
@article{ebrahimi2026targeting,
  title = {{Targeting NOTCH-immune crosstalk in gliomas: from mechanisms to therapeutics.}},
  author = {Safieh Ebrahimi and NoorMohammad Meshkinkhood and Ali Aliee and Li Yuhan and Maryam Koulivand and Zahra Koulivand and Ali Gorji},
  journal = {Frontiers in oncology},
  year = {2026},
  month = oct,
  doi = {10.3389/fonc.2026.1936605},
  url = {https://europepmc.org/article/MED/42909908},
  note = {CC BY},
}
RIS
TY  - JOUR
TI  - Targeting NOTCH-immune crosstalk in gliomas: from mechanisms to therapeutics.
AU  - Safieh Ebrahimi
AU  - NoorMohammad Meshkinkhood
AU  - Ali Aliee
AU  - Li Yuhan
AU  - Maryam Koulivand
AU  - Zahra Koulivand
AU  - Ali Gorji
PY  - 2026
DA  - 2026/10/07
JO  - Frontiers in oncology
DO  - 10.3389/fonc.2026.1936605
UR  - https://europepmc.org/article/MED/42909908
AB  - Glioblastoma (GBM) is a highly aggressive and treatment-resistant malignancy characterized by an immunosuppressive tumor microenvironment (TME) that promotes disease progression and poor clinical outcomes. Increasing evidence suggests that NOTCH signaling is a key regulator of GBM progression, governing both tumor cell plasticity and immune evasion. In addition to its roles in development and stem cell maintenance, NOTCH signaling modulates interactions among glioma stem-like cells, immune cells, and stromal components. NOTCH signaling in both tumor and stromal compartments modulates immune cell fate decisions, antigen presentation, and inflammatory cytokine expression. This suggests its potential role as a key modulator of immune crosstalk within the TME of GBM. Moreover, dysregulation of the NOTCH signaling pathway may lead to an immunosuppressive TME, enhance tumor heterogeneity, and restrict responses to conventional therapies. Recent investigations also reveal the epigenetic and non-coding RNA patterns that reinforce aberrant NOTCH activity in GBM. Understanding the multifaceted interactions among NOTCH signaling, oncogenic pathways, and immunomodulatory mechanisms could provide insights into the molecular pathogenesis of GBM progression. Here, we discuss the pleiotropic and context-dependent functions of NOTCH signaling in GBM, with particular emphasis on its implications for tumor-immune interactions and its potential as a therapeutic target to address immune escape and treatment resistance.
SN  - 2234-943X
ER  -