Metabolic reprogramming in triple-negative breast cancer through Myc suppression of TXNIP - Wikidata - wikimedia - TriplyDB

Metabolic reprogramming in triple-negative breast cancer through Myc suppression of TXNIP

Metabolic reprogramming in triple-negative breast cancer through Myc suppression of TXNIP

http://www.wikidata.org/entity/Q35567021

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The Quest for Targets Executing MYC-Dependent Cell Transformation Interactions between Myc and MondoA transcription factors in metabolism and tumourigenesis Key Players in Choline Metabolic Reprograming in Triple-Negative Breast Cancer ROS homeostasis and metabolism: a critical liaison for cancer therapy The Emerging Role of Thioredoxin-Interacting Protein in Myocardial Ischemia/Reperfusion Injury Attacking the supply wagons to starve cancer cells to death.The glucose-sensing transcription factor MLX promotes myogenesis via myokine signaling Inhibition of fatty acid oxidation as a therapy for MYC-overexpressing triple-negative breast cancer.MYC functions are specific in biological subtypes of breast cancer and confers resistance to endocrine therapy in luminal tumours.Effects of 1,25(OH)₂D₃ on Cancer Cells and Potential Applications in Combination with Established and Putative Anti-Cancer Agents.Non-invasive (89)Zr-Transferrin PET Shows Improved Tumor Targeting Compared to (18)F-FDG PET in MYC-overexpressing Human Triple Negative Breast Cancer.Metabolic profiling of triple-negative breast cancer cells reveals metabolic vulnerabilities.Targeting EphA2 impairs cell cycle progression and growth of basal-like/triple-negative breast cancers.Multilevel regulation of an α-arrestin by glucose depletion controls hexose transporter endocytosis.MYC-Driven Pathways in Breast Cancer Subtypes.Genome-scale regression analysis reveals a linear relationship for promoters and enhancers after combinatorial drug treatment.MYC and tumor metabolism: chicken and egg.Metabolic advantages and vulnerabilities in brain metastases.Multi-omic approach decodes paradoxes of the triple-negative breast cancer: lessons for predictive, preventive and personalised medicine.NDRG2 facilitates colorectal cancer differentiation through the regulation of Skp2-p21/p27 axis.Molecular Mechanisms and Emerging Therapeutic Targets of Triple-Negative Breast Cancer Metastasis.The anti-tumor efficacy of CDK4/6 inhibition is enhanced by the combination with PI3K/AKT/mTOR inhibitors through impairment of glucose metabolism in TNBC cells.Metabolite profiling identifies a signature of tumorigenicity in hepatocellular carcinoma.Near-simultaneous quantification of glucose uptake, mitochondrial membrane potential, and vascular parameters in murine flank tumors using quantitative diffuse reflectance and fluorescence spectroscopy.BET Bromodomain inhibition promotes De-repression of TXNIP and activation of ASK1-MAPK pathway in acute myeloid leukemia.Metabolic Targeting of Breast Cancer Cells With the 2-Deoxy-D-Glucose and the Mitochondrial Bioenergetics Inhibitor MDIVI-1

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Metabolic reprogramming in triple-negative breast cancer through Myc suppression of TXNIP

http://www.wikidata.org/entity/Q35567021

description

2015 nî lūn-bûn

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2015年の論文

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2015年論文

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2015年論文

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2015年論文

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2015年論文

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2015年論文

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2015年论文

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2015年论文

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2015年论文

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name

Metabolic reprogramming in triple-negative breast cancer through Myc suppression of TXNIP

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Metabolic reprogramming in triple-negative breast cancer through Myc suppression of TXNIP

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type

label

Metabolic reprogramming in triple-negative breast cancer through Myc suppression of TXNIP

@ast

Metabolic reprogramming in triple-negative breast cancer through Myc suppression of TXNIP

@en

prefLabel

Metabolic reprogramming in triple-negative breast cancer through Myc suppression of TXNIP

@ast

Metabolic reprogramming in triple-negative breast cancer through Myc suppression of TXNIP

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PNAS.1501555112

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Proceedings of the National Academy of Sciences of the United States of America

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Metabolic reprogramming in triple-negative breast cancer through Myc suppression of TXNIP

@en

P2093

Adam L Cohen

http://www.w3.org/2001/XMLSchema#string

Alana L Welm

http://www.w3.org/2001/XMLSchema#string

Blake R Wilde

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John M O'Shea

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Liangliang Shen

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Mohan R Kaadige

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Stéphanie Cunha

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Role of thioredoxin reductase 1 and thioredoxin interacting protein in prognosis of breast cancer

Mlx, a novel Max-like BHLHZip protein that interacts with the Max network of transcription factors

MondoA, a novel basic helix-loop-helix-leucine zipper transcriptional activator that constitutes a positive branch of a max-like network

Tumor grafts derived from women with breast cancer authentically reflect tumor pathology, growth, metastasis and disease outcomes

Coordination of nutrient availability and utilization by MAX- and MLX-centered transcription networks

Gene Expression Omnibus: NCBI gene expression and hybridization array data repository

A gene-expression signature as a predictor of survival in breast cancer

Melanoma metastasis suppression by chromosome 6: evidence for a pathway regulated by CRSP3 and TXNIP

Lactic acidosis triggers starvation response with paradoxical induction of TXNIP through MondoA

Triple-Negative Breast Cancer

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5425-5430

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10.1073/PNAS.1501555112

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17

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25870263

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4418882

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