Targeting the neural stem cells in subventricular zone for the treatment of glioblastoma: an update from preclinical evidence to clinical interventions

Li, Sijia; Dong, Li Min; Pan, Zhenyu; Yang, Guozi

doi:10.1186/s13287-023-03325-4

Cited by 6 publications

(3 citation statements)

References 74 publications

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“…Under physiological conditions, neural stem cells (NSCs) differentiate into neuroblasts, then neurons, oligodendrocytes, and astrocytes [ 24 ]. Neuroblasts play a significant role during embryonic development.…”

Section: Discussionmentioning

confidence: 99%

Neuroprotective Effect of Solid Lipid Nanoparticles Loaded with Lepidium sativum (L.) Seed Bioactive Components Enhance Bioavailability and Wnt/β-Catenin/Camk-II Signaling Cascade in SH-SY5Y Neuroblastoma Cells

Al-Saran,

Subash-Babu,

Al-Harbi

et al. 2024

Nanomaterials

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The primary pathological hallmark of Alzheimer’s disease (AD) is the formation and accumulation of neurofibrillary tangles and plaques, which result from the aggregation of amyloid-β (Aβ) induced by oxidative stress. The effectiveness of Alzheimer’s disease (AD) therapeutics significantly hinges on the drug’s bioavailability and its ability to penetrate neuronal cells. The current investigation was designed as a first attempt to examine bio-fabricated Lepidium sativum (LS) seed-extract-loaded solid lipid nanoparticles (SLNps) to increase bioavailability and bioefficacy for the prevention of undifferentiated SH-SY5Y neuronal cells from oxidative stress induced by H2O2 and amyloid-β peptide (Aβ,1-42). The SLNps were fabricated using LS extract as a water phase and hyaluronic acid and chia seed fatty acids as a lipid phase, then confirmed and characterized using UV, Zeta size, and SEM methods. The biological safety of synthesized LS-SLNps has been determined using MTT assay and PI staining (nuclear damage) in hMSCs. LS-SLNp-pretreated neuronal cells were induced with oxidative stress and 2 µM of beta-amyloid (Aβ,1-42) fibrils; furthermore, the neuroprotective potential of LS-SLNps was determined through the quenching of oxidative stress, enhancing mitochondrial oxidative capacity, and immunoregulatory potential. Observations found that cells treated with both H2O2 and beta-amyloid (Aβ,1-42) fibrils showed decreased neuronal cell growth, nuclear damage, and mitochondrial membrane potential due to oxidative stress. However, SH-SY5Y cells pretreated with LS-SLNps for 24 h showed an increase in cell proliferation with uniform morphology and increased mitochondrial membrane potential compared to cells pretreated with LS alone. Gene expression analysis found that LS-SLNps increased the expression of Wnt 3a and 5a, which stimulated the canonical, β-catenin, and non-canonical Camk-II expressions of nerve cell growth factors, confirming the molecular-level reversal of neurodegenerative diseases.

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Section: Discussionmentioning

confidence: 99%

Neuroprotective Effect of Solid Lipid Nanoparticles Loaded with Lepidium sativum (L.) Seed Bioactive Components Enhance Bioavailability and Wnt/β-Catenin/Camk-II Signaling Cascade in SH-SY5Y Neuroblastoma Cells

Al-Saran,

Subash-Babu,

Al-Harbi

et al. 2024

Nanomaterials

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“…Consequently, numerous retrospective studies have confirmed that GBs in close contact with the SVZ possess more aggressive patterns of recurrence and worse clinical outcomes [ 67 , 69 , 70 ]. Therefore, new therapy strategies are being assayed with the aim of targeting SVZ to eradicate NSCs or GSCs [ 71 ].…”

Section: Lessons Learned In the Pathophysiology Of Glioblastomamentioning

confidence: 99%

Glioblastoma Therapy: Past, Present and Future

Obrador,

Moreno-Murciano,

Oriol-Caballo

et al. 2024

IJMS

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Glioblastoma (GB) stands out as the most prevalent and lethal form of brain cancer. Although great efforts have been made by clinicians and researchers, no significant improvement in survival has been achieved since the Stupp protocol became the standard of care (SOC) in 2005. Despite multimodality treatments, recurrence is almost universal with survival rates under 2 years after diagnosis. Here, we discuss the recent progress in our understanding of GB pathophysiology, in particular, the importance of glioma stem cells (GSCs), the tumor microenvironment conditions, and epigenetic mechanisms involved in GB growth, aggressiveness and recurrence. The discussion on therapeutic strategies first covers the SOC treatment and targeted therapies that have been shown to interfere with different signaling pathways (pRB/CDK4/RB1/P16ink4, TP53/MDM2/P14arf, PI3k/Akt-PTEN, RAS/RAF/MEK, PARP) involved in GB tumorigenesis, pathophysiology, and treatment resistance acquisition. Below, we analyze several immunotherapeutic approaches (i.e., checkpoint inhibitors, vaccines, CAR-modified NK or T cells, oncolytic virotherapy) that have been used in an attempt to enhance the immune response against GB, and thereby avoid recidivism or increase survival of GB patients. Finally, we present treatment attempts made using nanotherapies (nanometric structures having active anti-GB agents such as antibodies, chemotherapeutic/anti-angiogenic drugs or sensitizers, radionuclides, and molecules that target GB cellular receptors or open the blood–brain barrier) and non-ionizing energies (laser interstitial thermal therapy, high/low intensity focused ultrasounds, photodynamic/sonodynamic therapies and electroporation). The aim of this review is to discuss the advances and limitations of the current therapies and to present novel approaches that are under development or following clinical trials.

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“…Therefore, comprehensive treatments such as radiotherapy and chemotherapy are often required to prolong patient survival [8,9]. Nevertheless, the recurrence rate remains high after treatment [10]. The average survival time for LGG patients is about ten years, while for HGG patients without treatment, this duration is less than 20 months [11], with only a small fraction of patients surviving more than three years after surgical treatment [12].…”

Section: Introductionmentioning

confidence: 99%

Overexpression of EZH2 is associated with clinicopathological parameters and poor prognosis in gliomas

Peng,

Chen,

Yang

et al. 2024

Preprint

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Histone methyltransferase EZH2, primarily localized in the nucleus, mediates constitutive Polycomb repressive complex activity by trimethylating lysine 27 of histone H3 (H3K27me3), leading to gene silencing through canonical and noncanonical mechanisms, resulting in transcriptional repression or activation. Its involvement is crucial in cell growth, proliferation, differentiation, and apoptosis, with its effects linked to the regulation of various targets and signaling pathways. Overexpression of EZH2 alters gene expression and function, thereby facilitating cancer progression. Recent research has identified the potential prognostic role of EZH2 expression in glioma patients. This study assesses the clinicopathological significance and prognostic value of EZH2 expression in gliomas using available data. The mRNA levels of EZH2 in tumor tissues and normal tissues were assessed using timer2.0 and data from CGCA and TGCA. The prognostic significance of EZH2 mRNA expression was determined using Kaplan-Meier plotter. A total of 147 clinical samples from glioma patients underwent immunohistochemistry analysis to evaluate EZH2 protein expression. Cox proportional hazards regression model and Kaplan-Meier survival curves were employed to assess the relationship between EZH2 expression, clinicopathological parameters, and overall survival (OS). Across multiple tumor cohorts, EZH2 was found to be upregulated and amplified in tumor tissues. In high-grade glioma patients, EZH2 expression was significantly increased, and higher EZH2 expression correlated with poorer OS, disease-specific survival (DSS), and progression-free interval (PFI). Therefore, the level of EZH2 may serve as a prognostic biomarker for glioma patients.

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Targeting the neural stem cells in subventricular zone for the treatment of glioblastoma: an update from preclinical evidence to clinical interventions

Cited by 6 publications

References 74 publications

Neuroprotective Effect of Solid Lipid Nanoparticles Loaded with Lepidium sativum (L.) Seed Bioactive Components Enhance Bioavailability and Wnt/β-Catenin/Camk-II Signaling Cascade in SH-SY5Y Neuroblastoma Cells

Neuroprotective Effect of Solid Lipid Nanoparticles Loaded with Lepidium sativum (L.) Seed Bioactive Components Enhance Bioavailability and Wnt/β-Catenin/Camk-II Signaling Cascade in SH-SY5Y Neuroblastoma Cells

Glioblastoma Therapy: Past, Present and Future

Overexpression of EZH2 is associated with clinicopathological parameters and poor prognosis in gliomas

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