Metabolic alterations in highly tumorigenic glioblastoma cells: preference for hypoxia and high dependency on glycolysis.
about
Salinomycin as a drug for targeting human cancer stem cellsCancer stem cell metabolismThe sweet trap in tumors: aerobic glycolysis and potential targets for therapyShort-Term Differentiation of Glioblastoma Stem Cells Induces Hypoxia Tolerance.Type 3 deiodinase: role in cancer growth, stemness, and metabolismOvarian cancer spheroid cells with stem cell-like properties contribute to tumor generation, metastasis and chemotherapy resistance through hypoxia-resistant metabolismAnalysis of the cytotoxicity of carbon-based nanoparticles, diamond and graphite, in human glioblastoma and hepatoma cell linesRegulation of stem-like cancer cells by glutamine through β-catenin pathway mediated by redox signaling.Requirement of ABC transporter inhibition and Hoechst 33342 dye deprivation for the assessment of side population-defined C6 glioma stem cell metabolism using fluorescent probesEstrogen Receptor β as a Therapeutic Target in Breast Cancer Stem Cells.High grade glioblastoma is associated with aberrant expression of ZFP57, a protein involved in gene imprinting, and of CPT1A and CPT1C that regulate fatty acid metabolismBreast cancer stem cells rely on fermentative glycolysis and are sensitive to 2-deoxyglucose treatment.Neural stem/progenitor cells display a low requirement for oxidative metabolism independent of hypoxia inducible factor-1alpha expression.Ovarian tumor-initiating cells display a flexible metabolismMetabolic regulation of cancer cell side population by glucose through activation of the Akt pathway.Inhibition of oxidative metabolism leads to p53 genetic inactivation and transformation in neural stem cells.PERK silence inhibits glioma cell growth under low glucose stress by blockage of p-AKT and subsequent HK2's mitochondria translocation.Targeting the facilitative glucose transporter GLUT1 inhibits the self-renewal and tumor-initiating capacity of cancer stem cells.Hypoxia promotes isocitrate dehydrogenase-dependent carboxylation of α-ketoglutarate to citrate to support cell growth and viabilityElevated NIBP/TRAPPC9 mediates tumorigenesis of cancer cells through NFκB signalingTargeted therapy against cancer stem cells.Hyperbaric oxygen promotes malignant glioma cell growth and inhibits cell apoptosis.Cancer Stem Cells in Small Cell Lung Cancer Cell Line H446: Higher Dependency on Oxidative Phosphorylation and Mitochondrial Substrate-Level Phosphorylation than Non-Stem Cancer CellsTherapeutic Strategy for Targeting Aggressive Malignant Gliomas by Disrupting Their Energy Balance.Metabolic activation of mitochondria in glioma stem cells promotes cancer development through a reactive oxygen species-mediated mechanism.Lactate dehydrogenase-A inhibition induces human glioblastoma multiforme stem cell differentiation and deathGlycemic modulation in neuro-oncology: experience and future directions using a modified Atkins diet for high-grade brain tumors.In Vivo Loss of Function Screening Reveals Carbonic Anhydrase IX as a Key Modulator of Tumor Initiating Potential in Primary Pancreatic Tumors.Metabolic Reprogramming and Dependencies Associated with Epithelial Cancer Stem Cells Independent of the Epithelial-Mesenchymal Transition Program.Identification of novel hypoxia response genes in human glioma cell line a172.Mitochondrial DNA mutations and breast tumorigenesis.The identification of mitochondrial DNA variants in glioblastoma multiforme.Exploring the differences in metabolic behavior of astrocyte and glioblastoma: a flux balance analysis approach.The metabolic landscape of cancer stem cells.Loss of fructose-1,6-bisphosphatase induces glycolysis and promotes apoptosis resistance of cancer stem-like cells: an important role in hexavalent chromium-induced carcinogenesis.Cancer stem cells, metabolism, and therapeutic significance.Laminin-adherent versus suspension-non-adherent cell culture conditions for the isolation of cancer stem cells in the DAOY medulloblastoma cell line.Cancer stem cell molecular reprogramming of the Warburg effect in glioblastomas: a new target gleaned from an old concept.Targeting cancer stem-like cells in glioblastoma and colorectal cancer through metabolic pathways.Control of glioma cell death and differentiation by PKM2-Oct4 interaction.
P2860
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P2860
Metabolic alterations in highly tumorigenic glioblastoma cells: preference for hypoxia and high dependency on glycolysis.
description
2011 nî lūn-bûn
@nan
2011 թուականի Յուլիսին հրատարակուած գիտական յօդուած
@hyw
2011 թվականի հուլիսին հրատարակված գիտական հոդված
@hy
2011年の論文
@ja
2011年学术文章
@wuu
2011年学术文章
@zh-cn
2011年学术文章
@zh-hans
2011年学术文章
@zh-my
2011年学术文章
@zh-sg
2011年學術文章
@yue
name
Metabolic alterations in highl ...... high dependency on glycolysis.
@ast
Metabolic alterations in highl ...... high dependency on glycolysis.
@en
type
label
Metabolic alterations in highl ...... high dependency on glycolysis.
@ast
Metabolic alterations in highl ...... high dependency on glycolysis.
@en
prefLabel
Metabolic alterations in highl ...... high dependency on glycolysis.
@ast
Metabolic alterations in highl ...... high dependency on glycolysis.
@en
P2093
P2860
P356
P1476
Metabolic alterations in highl ...... high dependency on glycolysis.
@en
P2093
Marcia Ogasawara
Peng Huang
Seiji Kondo
Takashi Shingu
Yunfei Zhou
P2860
P304
32843-32853
P356
10.1074/JBC.M111.260935
P407
P577
2011-07-27T00:00:00Z