Metabolic alterations in highly tumorigenic glioblastoma cells: preference for hypoxia and high dependency on glycolysis. - Wikidata - wikimedia - TriplyDB

Metabolic alterations in highly tumorigenic glioblastoma cells: preference for hypoxia and high dependency on glycolysis.

Metabolic alterations in highly tumorigenic glioblastoma cells: preference for hypoxia and high dependency on glycolysis.

http://www.wikidata.org/entity/Q35213377

about

Salinomycin as a drug for targeting human cancer stem cells Cancer stem cell metabolism The sweet trap in tumors: aerobic glycolysis and potential targets for therapy Short-Term Differentiation of Glioblastoma Stem Cells Induces Hypoxia Tolerance.Type 3 deiodinase: role in cancer growth, stemness, and metabolism Ovarian cancer spheroid cells with stem cell-like properties contribute to tumor generation, metastasis and chemotherapy resistance through hypoxia-resistant metabolism Analysis of the cytotoxicity of carbon-based nanoparticles, diamond and graphite, in human glioblastoma and hepatoma cell lines Regulation 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 probes Estrogen 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 metabolism Breast 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 metabolism Metabolic 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 viability Elevated NIBP/TRAPPC9 mediates tumorigenesis of cancer cells through NFκB signaling Targeted 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 Cells Therapeutic 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 death Glycemic 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.

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Metabolic alterations in highly tumorigenic glioblastoma cells: preference for hypoxia and high dependency on glycolysis.

http://www.wikidata.org/entity/Q35213377

description

2011 nî lūn-bûn

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2011 թուականի Յուլիսին հրատարակուած գիտական յօդուած

@hyw

2011 թվականի հուլիսին հրատարակված գիտական հոդված

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2011年の論文

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2011年学术文章

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2011年学术文章

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2011年学术文章

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2011年学术文章

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2011年学术文章

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2011年學術文章

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Metabolic alterations in highl ...... high dependency on glycolysis.

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Metabolic alterations in highl ...... high dependency on glycolysis.

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type

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Metabolic alterations in highl ...... high dependency on glycolysis.

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Metabolic alterations in highl ...... high dependency on glycolysis.

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Journal of Biological Chemistry

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Li Feng

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Marcia Ogasawara

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Peng Huang

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Seiji Kondo

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Takashi Shingu

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Yunfei Zhou

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Zhao Chen

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P2860

Prospective identification of tumorigenic breast cancer cells

A HIF1alpha regulatory loop links hypoxia and mitochondrial signals in pheochromocytomas

Glioma stem cells promote radioresistance by preferential activation of the DNA damage response

On the Origin of Cancer Cells

Identification of a cancer stem cell in human brain tumors

A cell initiating human acute myeloid leukaemia after transplantation into SCID mice

Mitochondrial tumour suppressors: a genetic and biochemical update

Succinate links TCA cycle dysfunction to oncogenesis by inhibiting HIF-alpha prolyl hydroxylase

A perivascular niche for brain tumor stem cells

The ABC transporter Bcrp1/ABCG2 is expressed in a wide variety of stem cells and is a molecular determinant of the side-population phenotype

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