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Objectives: Our study aimed to explore the effects of quercetin on glioma stem cells in patients with brain tumors.
Methods: Human glioblastoma cell line, U373MG, or glioma stem cell lines, were treated with quercetin. Cell viability was determined by using the cell counting kit 8 assays. Cell apoptosis was determined by using the Annexin- V reagent. Western blotting and qPCR were used to detect the protein and mRNA levels of cyclindependent kinase inhibitor 2A (p16INK4a). Chromatin immunoprecipitation analysis was used to determine the enrichment of H3K27me3 on the p16-INK4 locus with or without quercetin.
Results: Treatment with quercetin inhibited cell viability and induced cell apoptosis in U373MG cells. Moreover, treatment with quercetin inhibited the cell viability of four glioma stem cell lines (G3, G10, G15, and G17) from brain tumor samples at high concentrations while having no obvious effects for the other two glioma stem cell lines (G9 and G21). Treatment with quercetin increased the mRNA and protein levels of p16- INK4 in glioma stem cell lines. The study of the underlying mechanism revealed that treatment with quercetin reduced H3K27me3 (an epigenetic modification to the DNA packaging protein histone H3) levels at the p16-INK4 locus.
Conclusions: In conclusion, quercetin inhibits glioma cell growth by activating p16-INK4 gene expression through epigenetic regulation.
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http://dx.doi.org/10.2174/0118715206332048241126095207 | DOI Listing |
Adv Healthc Mater
September 2025
School of Biological and Health Systems Engineering (SBHSE), Arizona State University, Tempe, AZ, 85287, USA.
The prognosis of glioblastoma multiforme (GBM) remains dismal, despite standard treatment regimens. A key challenge in treating GBM is the persistence of glioma stem cells (GSCs) within the perivascular niche (PVN) - a protective tumor microenvironment (TME) that is often associated with inadequate drug penetration. Current preclinical models do not capture complexity of the human TME, particularly the vasculature and niche-specific interactions that drive GBM progression.
View Article and Find Full Text PDFPhotodiagnosis Photodyn Ther
September 2025
Wellman Center for Photomedicine, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
One of the key factors contributing to the poor prognosis of glioblastoma is the treatment resistance of glioma stem cells (GSCs). In this study, the efficacy of photodynamic therapy (PDT) using talaporfin sodium (NPe6), a second-generation photosensitizer, in combination with a semiconductor laser approved for clinical use in Japan was evaluated. The evaluation was performed in a patient-derived glioma stem cell (GSC) line, MGG8, which was established from human glioblastoma tissue.
View Article and Find Full Text PDFCell Rep
September 2025
Virginia Tech Fralin Biomedical Research Institute Cancer Research Center DC, Children's National Research & Innovation Campus, Washington, DC, USA; Department of Biomedical Sciences and Pathobiology (DBSP), Virginia-Maryland College of Veterinary Medicine, Virginia Tech, Blacksburg, VA, USA; Center
Nuclear receptor binding set domain protein 1 (NSD1) is a key histone methyltransferase that catalyzes di-methylation of lysine 36 of histone H3 (H3K36me2), essential for active chromatin domains. While the loss of NSD1 activity halts embryonic development and its aberrant gain drives oncogenesis in leukemia and glioma, the regulatory mechanisms remain poorly understood. Here, we uncover that NSD1 requires allosteric activation through the aromatic pocket of its Pro-Trp-Trp-Pro 2 (PWWP2) domain.
View Article and Find Full Text PDFJ Cell Mol Med
September 2025
Department of Neurosurgery, Taihe Hospital, Hubei University of Medicine, Shiyan City, Hubei Province, China.
Glioblastoma (GBM) exhibits remarkable intra-tumoral heterogeneity, which contributes to therapeutic resistance and poor clinical outcomes. In this study, we employed integrative single-cell RNA sequencing analysis across two complementary public datasets encompassing diverse cellular populations from GBM centre and periphery regions to elucidate potential spatial molecular programmes driving tumour progression. Our analyses revealed substantial transcriptomic divergence between anatomically distinct tumour regions, with NUCB2 emerging as significantly upregulated in centre-residing neural progenitor cell-like (NPC-like) tumour cells.
View Article and Find Full Text PDFOncol Rep
November 2025
Department of Neurosurgery, The First Hospital of Lanzhou University, Lanzhou, Gansu 730000, P.R. China.
Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that the control GADPH western blots shown in Fig. 5D were strikingly simillar to three lanes in the GAPDH panel shown in Fig. 4D, even though the experimental conditions reported in these figure parts were different, suggesting that one of these figures may have been assembled incorrectly.
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