Berberine inhibits glioma cell migration and invasion by suppressing TGF-β1/COL11A1 pathway.
In previous studies, we demonstrated that berberine inhibits glioma cell proliferation by inhibiting mutant p53 protein and promoting mitochondrial damage.
Brain Cancer · LIVING RESEARCH LIBRARY
Ongoing Research for Brain Cancer Using Advanced Alternative Medicine
Explore positive published findings by substance, cancer biology, treatment interaction and quality-of-life outcome.
Every entry includes the original study title, year, concise finding and a direct PubMed link.
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Research organized by substance and finding
Browse 30 source-linked studies with the full title, publication year, research focus and a concise finding. Select any linked substance to move directly to its corresponding Sunridge page.
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Anti-glioblastoma effects of nanomicelle-curcumin plus erlotinib.
Furthermore, the level of proteins related to angiogenesis and Wnt pathway-associated genes in the nanomicelle-curcumin + erlotinib group were significantly decreased compared to the curcumin, erlotinib, and control groups.
Curcumin Analogs in Glioblastoma Therapy: A Narrative Review.
Preclinical studies have demonstrated the efficacy of curcumin analogs, including C-150, ALZ003, and DMC-BH, in inhibiting GBM growth, angiogenesis, and improving survival in orthotopic and xenograft mouse models.
Curcumin combining temozolomide formed localized nanogel for inhibition of postsurgical chemoresistant glioblastoma.
Estimated survival characteristics demonstrated that the nanogel could play a significant role in TMZ-resistant tumor inhibition with low drug-induced toxicity.
Effect of curcumin on glioblastoma cells.
In conclusion, we have shown that nano micelles curcumin effectively prevent proliferation, and invasion of GBM cells through perturbation of Wnt/β-catenin and NF-κB pathways, suggesting further investigations on the therapeutic application of this novel anticancer drug in in vivo models.
A combination of metformin and epigallocatechin gallate potentiates glioma chemotherapy in vivo.
Our triple-drug combination therapy significantly inhibited tumor growth in vivo and increased the survival rate (50%) of rats when compared with individual or dual treatments.
Epigallocatechin-3-Gallate Suppresses Glioma by Targeting Integrin αvβ3/FAK/ERK Signaling Axis and Matrix Metalloproteinases.
EGCG inhibited cell proliferation with IC50 values of 127.8 μM (U87), 172.9 μM (U251), and 104.7 μM (LN229) in glioma cells, while inducing apoptosis.
The synergistic anti-Warburg efficacy of temozolomide, metformin and epigallocatechin gallate in glioblastoma.
Based on this lacuna, the current study aimed to explore the therapeutic efficacy of the triple-drug combination of temozolomide, metformin and epigallocatechin gallate in attenuating Warburg effect and glucose uptake in glioblastoma both in vitro and in vivo.
Ginsenoside Rg5 inhibits glioblastoma by activating ferroptosis via NR3C1/HSPB1/NCOA4.
We aim to study whether ginsenoside Rg5 exerted inhibitory effects on crucial aspects of glioma stem cells, including cell viability, tumor initiation, invasion, self-renewal ability, neurosphere formation, and stemness.
Curzerene suppresses progression of human glioblastoma through inhibition of glutathione S-transferase A4.
Curzerene was found to inhibit the expression of GSTA4 mRNA and protein in U251 and U87 glioma cells, and this effect correlated with a downregulation of the proliferation of these cells in a time- and dose-dependent manner.
Intranasal Delivery of Ivermectin Nanosystems as an Antitumor Agent: Focusing on Glioma Suppression.
Nanoencapsulated IVM significantly reduced the viability of various cancer cell lines, particularly glioma cell lines, which led us to evaluate them in a preclinical glioma model.
A natural compound melatonin enhances the effects of Nimotuzumab via inhibiting EGFR in glioblastoma.
This proposition was validated in our in vitro and in vivo studies where melatonin synergistically augmented cytotoxicity and apoptosis in Nimotuzumab-treated glioma cells.
Glioblastoma progression is hindered by melatonin-primed mesenchymal stromal cells through dynamic intracellular and extracellular reorganizations.
This study investigates how MSCs influence tumor behavior and explores the synergistic anticancer effects in combination with melatonin (Mel).
Hierarchical Disruption of the Tryptophan-Melatonin Axis Contributes to Glioma Progression Through AKT/ERK/STAT3 Signalling.
Restoration of these factors suppressed glioma cell proliferation, migration and invasion while promoting apoptosis.
Inhibition of autophagy triggers melatonin-induced apoptosis in glioblastoma cells.
Remarkably, co-treatment with 3-MA and melatonin significantly enhanced the apoptotic cell population in the glioblastoma cells, along with a prominent decrease in the expression of bcl-2 and increase in the Bax expression levels, which collectively indicated that the disruption of autophagy triggers the melatonin-induced apoptosis in glioblastoma cells.
Melatonin Synergises the Chemotherapeutic Effect of Temozolomide in Glioblastoma by Suppressing NF-κB/COX-2 Signalling Pathways.
Melatonin (Mel), a natural indoleamine synthesised by the pineal gland, has demonstrated synergistic anti-tumour effects when combined with various chemotherapy agents in multiple studies.
Human microbiota influence the immune cell composition and gene expression in the tumor environment of a murine model of glioma.
We have previously found that, when using gnotobiotic mice transplanted with human fecal microbiota, the gut microbial composition influenced the response to anti-PD-1 in a mouse model of glioma.
Quercetin and Glioma: Which Signaling Pathways are Involved?
Multiple lines of evidence have shown that Quercetin has anti-tumor effects, documenting this natural compound exerts its pharmacological effects by targeting a variety of cellular and molecular processes, i.e., apoptosis, metastasis, and autophagy.
Quercetin Induces Apoptosis in Glioblastoma Cells by Suppressing Axl/IL-6/STAT3 Signaling Pathway.
Quercetin treatment significantly reduced cell viability in two GBM cell lines of U87MG and U373MG while keeping 85% of normal astrocytes alive.
Quercetin induces MGMT+ glioblastoma cells apoptosis via dual inhibition of Wnt3a/β-Catenin and Akt/NF-κB signaling pathways.
Quercetin significantly suppressed the growth and migration of human GBM T98G cells, induced apoptosis, and arrested cells in the S-phase cell cycle.
Quercetin Inhibits Glioblastoma Growth and Prolongs Survival Rate through Inhibiting Glycolytic Metabolism.
We found that quercetin administration inhibited GBM cell proliferation and promoted cell apoptosis in vitro.
Quercetin Suppresses Human Glioblastoma Migration and Invasion via GSK3β/β-catenin/ZEB1 Signaling Pathway.
Our results showed that quercetin markedly suppressed the viability of glioblastoma cells in vitro and in vivo, and significantly inhibited glioblastoma cell migration and invasion.
Mammalian target of rapamycin inhibition protects glioma cells from temozolomide-induced cell death.
Additionally, we employed a novel translatomic based mass spectrometry approach ("mePROD") to analyze acute changes in translated proteins. mTOR inhibition with rapamycin protected glioblastoma cells from temozolomide toxicity.
Effect of gold-conjugated resveratrol nanoparticles on glioma cells and its underlying mechanism.
Rsv-AuNPs treatment significantly suppressed proliferation, migration, and invasion of U87 cells (all P < 0.05) and increased the apoptosis rate (P < 0.05).
Resveratrol as a Novel YAP Inhibitor Targeting Glioblastoma Progression and Sensitizing to Chemotherapy.
Resveratrol (RV), a natural blood-brain barrier-permeable compound, was evaluated for growth inhibition and YAP-targeted effects.
Protective effects of silymarin in glioblastoma cancer cells through redox system regulation.
Silymarin, a flavonoid extracted from milk thistle, has shown therapeutic potential in inhibiting cancer cell growth, promoting apoptosis, and reducing inflammation.
Sustained release of silibinin-loaded chitosan nanoparticle induced apoptosis in glioma cells.
In this study, a chitosan nanoparticle formulation was synthesized for loading silibinin as a sustained-release drug system to evaluate its effects on apoptosis in C6 glioma cells.
Sulforaphane induces cell morphology change and cell apoptosis by activating endoplasmic reticulum stress in glioblastoma.
This study aimed to elucidate the role and underlying molecular mechanisms of SFN in regulating GBM progression, particularly through the endoplasmic reticulum stress (ERS) and unfolded protein response (UPR) pathways.
Glioblastoma Invasiveness and Collagen Secretion Are Enhanced by Vitamin C.
Finally, orthotopic xenografts induced in immunocompetent guinea pigs showed that vitamin C deficiency retained collagen, reduced blood vessel invasion, and affected glomeruloid vasculature formation, all pathological conditions associated with malignancy.
Molecular Determinants of Calcitriol Signaling and Sensitivity in Glioma Stem-like Cells.
Recently, we have shown that the in vitro and ex vivo treatment of glioblastoma stem-like cells with the hormonally active form of vitamin D3, calcitriol (1α,25(OH)2-vitamin D3) can block stemness in a subset of cell lines and reduce tumor growth.
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