Cancer, Hypoxia, and Metabolism

This study identifies two resistance mechanisms to LDH inhibitors in complex I-mutant HTC models through forward genetic screens.

This study investigates how NF1 deficiency affects metabolic reprogramming in ER+ breast cancer and identifies potential therapeutic synergies between metabolic and targeted inhibitors.

This study shows that malignant glioma cells rely on amino acid and glucose fermentation for ATP production, not oxidative phosphorylation, and that glutamine is essential for maintaining ATP content and viability.

The paper analyzes hypoxia-related gene expression in cancers from anatomically similar locations using TCGA data to identify prognostic hub genes and functional enrichments.

The paper classifies metastatic potentials in cancer cell lines using HIF1 downstream gene expression patterns across 30 cancer types.

This study shows IFN-γ reduces tumour growth by increasing glycolysis and lactate production through NO-dependent mechanisms, with implications for cancer immunotherapy.

This study shows lactate activates the mitochondrial electron transport chain without being metabolized, suppressing glycolysis and enhancing oxidative phosphorylation in various cell types.

The paper evaluates mitochondrial OXPHOS expression and function across murine tumors and normal tissues, finding lower OXPHOS levels in tumors compared to normal and high OXPHOS organs.

The paper identifies metabolic reaction modules driving metastatic transitions in ovarian cancer and validates oseltamivir as a non-cytotoxic drug to disrupt spheroidal morphologies.

This study identifies lactate-driven histone lactylation as a mechanism enhancing c-Myc expression and promoting breast cancer progression through SRSF10-mediated alternative splicing.

This study uses TCGA transcriptomics data to analyze metabolic shifts in 11 cancer subtypes and their adjacent normal tissues, revealing patterns in glucose uptake, glycolysis, TCA cycle, and glutaminolysis.

This study identifies upregulated mitochondrial one-carbon metabolism in anaplastic thyroid cancer as a targetable vulnerability, showing that inhibiting SHMT2 reduces proliferation and tumor growth.

This study identifies two metabolic subtypes of endometrial cancer using transcriptomics and metabolic modeling, linking them to clinical outcomes and genomic alterations.

This paper reviews strategies for designing biomaterials that simulate or induce hypoxic conditions to stabilize HIF for biomedical applications, particularly in cancer research.

This study shows dexamethasone inhibits HIF-1α stabilization and reduces GLUT1 expression in lipopolysaccharide-stimulated macrophages, impairing glucose uptake and metabolic reprogramming.

This paper develops a hybrid computational model of breast cancer-associated fibroblasts to identify HIF-1 as a driver of the reverse Warburg effect.

This study identifies 201 potential HIF1A cofactors in hypoxic cancer cells, with 30 validated and 21 matching known cofactors from public databases.

The paper profiles the metabolome of 180 cancer cell lines and identifies two major metabolic types linked to epithelial-mesenchymal transition (EMT).

The paper uses computational modeling and transcriptomic data to show that cancer cell phenotypes can be explained by Fenton reaction-driven proton production and reprogrammed metabolisms.

The paper develops hypoxia classifiers using decision trees from a meta-analysis of RNA-seq data, achieving high accuracy in identifying hypoxic samples across diverse datasets.

The paper identifies a HIF-1-independent hypoxia response pathway in C. elegans mediated by NHR-49, showing its role in hypoxia survival and gene regulation.

This study shows hypoxia and HIF regulate chromatin accessibility through locus-specific changes, which are reversible and can be mimicked by HIF stabilisation.

This study investigates tumor-stromal metabolic interactions in colorectal cancer by integrating constraint-based models with metabolomics data, revealing how cancer-associated fibroblasts reprogram tumor cell metabolism.

The paper identifies crosstalk between SKN-1/NRF and HIF-1 in C. elegans, showing SKN-1 inhibits HIF-1 through EGL-9 regulation.

This study identifies novel hypoxia-inducible genes through a meta-analysis of transcriptomes and bibliome data, revealing previously uncharacterized genes like G protein-coupled receptor 146.

The paper develops a bioinformatics pipeline to integrate multi-omics data into personalized genome-scale metabolic models, identifying redox metabolism targets in radiation-resistant tumors.

The paper identifies a drug-tolerant metabolic state in melanoma cells that reduces both glycolysis and oxidative phosphorylation, supporting survival but limiting growth.

The paper shows DNA methylation prevents HIF binding, affecting hypoxia responses and tumour immunotolerance.

The paper shows that AKT, but not MYC, causes cell death in oxidative conditions by increasing reactive oxygen species, revealing a metabolic vulnerability in cancer cells.

This study performs a meta-analysis of hypoxic transcriptomes from public databases to identify common hypoxia-responsive genes and pathways.