FAM129A promotes self-renewal and maintains invasive status via stabilizing the Notch intracellular domain in glioma stem cells

Liu, Guohao; Zhang, Po; Chen, Sui; Chen, Zirong; Qiu, Yue; Peng, Peng; Huang, Wenda; Cheng, Fang; Zhang, Yang; Li, Huan; Xiao, Qungen; Mao, Feng; Wang, Baofeng; Jiang, Xueshi; Wan, Feng; Guo, Dong‐Sheng; Yu, Xingjiang

doi:10.1093/neuonc/noad079

Cited by 4 publications

(1 citation statement)

References 30 publications

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“…FAM129A is a positive regulator of Notch signaling through binding to NICD1. Targeting FAM129A inhibits GSC selfrenewal [123]. Simultaneous inhibition of Notch and Wnt/β-catenin pathway in GSCs with elevated ASCL1 expression promotes significant neuronal differentiation while suppressing the clonogenic potential [124].…”

Section: Regulation Of Stemnessmentioning

confidence: 99%

Mechanism of Notch Signaling Pathway in Malignant Progression of Glioblastoma and Targeted Therapy

Wang,

Gu,

Chen

et al. 2024

Biomolecules

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Glioblastoma multiforme (GBM) is the most aggressive form of glioma and the most common primary tumor of the central nervous system. Despite significant advances in clinical management strategies and diagnostic techniques for GBM in recent years, it remains a fatal disease. The current standard of care includes surgery, radiation, and chemotherapy, but the five-year survival rate for patients is less than 5%. The search for a more precise diagnosis and earlier intervention remains a critical and urgent challenge in clinical practice. The Notch signaling pathway is a critical signaling system that has been extensively studied in the malignant progression of glioblastoma. This highly conserved signaling cascade is central to a variety of biological processes, including growth, proliferation, self-renewal, migration, apoptosis, and metabolism. In GBM, accumulating data suggest that the Notch signaling pathway is hyperactive and contributes to GBM initiation, progression, and treatment resistance. This review summarizes the biological functions and molecular mechanisms of the Notch signaling pathway in GBM, as well as some clinical advances targeting the Notch signaling pathway in cancer and glioblastoma, highlighting its potential as a focus for novel therapeutic strategies.

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Section: Regulation Of Stemnessmentioning

confidence: 99%

Mechanism of Notch Signaling Pathway in Malignant Progression of Glioblastoma and Targeted Therapy

Wang,

Gu,

Chen

et al. 2024

Biomolecules

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BRD4 Degradation Enhanced Glioma Sensitivity to Temozolomide by Regulating Notch1 via Glu‐Modified GSH‐Responsive Nanoparticles

Yi,

Zhang,

Zhou

et al. 2024

Advanced Science

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Temozolomide (TMZ) serves as the principal chemotherapeutic agent for glioma; nonetheless, its therapeutic efficacy is compromised by the rapid emergence of drug resistance, the inadequate targeting of glioma cells, and significant systemic toxicity. ARV‐825 may play a role in modulating drug resistance by degrading the BRD4 protein, thereby exerting anti‐glioma effects. Therefore, to surmount TMZ resistance and achieve efficient and specific drug delivery, a dual‐targeted glutathione (GSH)‐responsive nanoparticle system (T+A@Glu‐NP) is designed and synthesized for the co‐delivery of ARV‐825 and TMZ. As anticipated, T+A@Glu‐NPs significantly enhanced penetration of the blood‐brain barrier (BBB), facilitated drug uptake by glioma cells, and exhibited efficient accumulation in brain tissue. Additionally, T+A@Glu‐NPs exhibited augmented efficacy against glioma both in vitro and in vivo through the induction of apoptosis, inhibition of proliferation, and cell cycle arrest. Furthermore, mechanistic exploration revealed that T+A@Glu‐NPs degraded the BRD4 protein, leading to the downregulation of Notch1 gene transcription and the inhibition of the Notch1 signaling pathway, thereby augmenting the therapeutic efficacy of glioma chemotherapy. Taken together, the findings suggest that T+A@Glu‐NPs represents a novel and promising therapeutic strategy for glioma chemotherapy.

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Cancer stem cells: advances in knowledge and implications for cancer therapy

Chu,

Tian,

Ning

et al. 2024

Sig Transduct Target Ther

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Cancer stem cells (CSCs), a small subset of cells in tumors that are characterized by self-renewal and continuous proliferation, lead to tumorigenesis, metastasis, and maintain tumor heterogeneity. Cancer continues to be a significant global disease burden. In the past, surgery, radiotherapy, and chemotherapy were the main cancer treatments. The technology of cancer treatments continues to develop and advance, and the emergence of targeted therapy, and immunotherapy provides more options for patients to a certain extent. However, the limitations of efficacy and treatment resistance are still inevitable. Our review begins with a brief introduction of the historical discoveries, original hypotheses, and pathways that regulate CSCs, such as WNT/β-Catenin, hedgehog, Notch, NF-κB, JAK/STAT, TGF-β, PI3K/AKT, PPAR pathway, and their crosstalk. We focus on the role of CSCs in various therapeutic outcomes and resistance, including how the treatments affect the content of CSCs and the alteration of related molecules, CSCs-mediated therapeutic resistance, and the clinical value of targeting CSCs in patients with refractory, progressed or advanced tumors. In summary, CSCs affect therapeutic efficacy, and the treatment method of targeting CSCs is still difficult to determine. Clarifying regulatory mechanisms and targeting biomarkers of CSCs is currently the mainstream idea.

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FAM129A promotes self-renewal and maintains invasive status via stabilizing the Notch intracellular domain in glioma stem cells

Cited by 4 publications

References 30 publications

Mechanism of Notch Signaling Pathway in Malignant Progression of Glioblastoma and Targeted Therapy

Mechanism of Notch Signaling Pathway in Malignant Progression of Glioblastoma and Targeted Therapy

BRD4 Degradation Enhanced Glioma Sensitivity to Temozolomide by Regulating Notch1 via Glu‐Modified GSH‐Responsive Nanoparticles

Cancer stem cells: advances in knowledge and implications for cancer therapy

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