Cancer, Hypoxia, and Metabolism

THER is a web tool that integrates hypoxia-related transcriptomic data to analyze tumor hypoxia mechanisms and drug responses.

The paper identifies PHD2 mutations that affect N-terminal prolyl-hydroxylation of HIF1α, challenging the belief that this site is dispensable for oxygen-dependent degradation.

This study identifies STAMBPL1's role in promoting angiogenesis in triple-negative breast cancer by activating the GRHL3/HIF1A/VEGFA axis through interaction with FOXO1.

This study links EPAS1HIF2 genetic adaptations in high-altitude populations to similar mutations in hypoxia-driven tumors, showing shared mechanisms in hypoxia response and tumorigenesis.

The paper shows HIF-1α regulates glycolytic shifts and mitochondrial function differently in bone marrow-derived macrophages compared to tissue-resident alveolar macrophages.

This study shows that low extracellular pH reduces ammonia toxicity in cancer cells by mitigating its cytotoxic effects.

This study shows oxygen-carrying nanoemulsions and respiratory hyperoxia reduce tumor hypoxia, enhance T cell and NK cell infiltration, and improve cancer immunotherapy outcomes.

The paper shows that lipid metabolism, specifically through OA, shifts metabolic pathways in breast cells, increasing SAM and 2-HG, which contribute to oncogenic properties and epigenetic changes.

This study shows that deleting HKDC1 in intestinal epithelial cells reduces tumor growth and protects against colorectal cancer in mice by impairing mitochondrial function and cell proliferation.

This paper challenges the conventional view of HIFs as mediators of hypoxic stress, proposing instead that HIFs prevent hypoxia by regulating electron transport and redefining the Warburg effect as a homeostatic response to metabolic demand.

This study identifies serine synthesis as a metabolic vulnerability in sunitinib-resistant renal cell carcinoma, showing that inhibiting key enzymes enhances drug sensitivity.

This study uses multiomic analysis to investigate metabolic interactions between colorectal cancer cells and hepatocytes in liver metastasis, revealing metabolic shifts and potential therapeutic targets.

This study shows that inhibiting glutaminase and xCT in TNBC disrupts redox balance, enhances chemotherapy efficacy, and can be monitored non-invasively using PET.

This study identifies TFE3 fusions driving OXPHOS in tRCC and reveals EGLN1 inhibition as a therapeutic target.

This paper identifies Sima/Hif1 as a critical factor for establishing the larval glycolytic program in Drosophila, showing it works with dERR to regulate metabolism during development.

The paper integrates computational metabolic modeling with experimental validation to identify hexokinase as a therapeutic target in colorectal cancer by analyzing CAF-conditioned tumor organoids.

This study shows that leukemia cells rely on increased mitochondrial respiration for survival when glucose uptake is acutely inhibited by KL-11743.

This study identifies hypoxia and glucose deprivation as drivers of aggressiveness in bladder cancer through metabolic adaptation and altered glycosylation.

This study identifies prognostic genes related to glucose metabolism in breast cancer and develops a model linking metabolism and immune infiltration, validated through experiments and single-cell analysis.

This study shows TIPE promotes glycolysis and stemness in melanoma by interacting with PKM2 and activating HIF-1α through phosphorylation.

This study shows that inhibiting PFKFB3 enhances the effectiveness of EGFR-TKIs by disrupting metabolic adaptations and DNA repair in drug-tolerant lung cancer cells.

This study combines mitochondrial-targeting anthelmintics with a GLUT1 inhibitor to target cancer metabolism, showing enhanced efficacy by disrupting both glycolysis and mitochondrial respiration in breast cancer cells.

This study shows CPI-613 reduces tumor growth in chemoresistant ovarian tumors by inhibiting mitochondrial function and enhancing chemotherapy response.

This study shows PFKP promotes lung cancer progression by interacting with the AXL-MET pathway, beyond its metabolic role in glycolysis.

This study shows that HER2-driven mammary tumors have reduced mitochondrial content but increased respiration, suggesting HER2 signaling enhances mitochondrial bioenergetics independently of mitochondrial content.

This study shows copper drives metabolic remodeling and progression in clear cell renal cell carcinoma by coordinating bioenergy, biosynthesis, and redox homeostasis.

This study identifies branched chain α-ketoacids (BCKAs) as novel signaling metabolites that activate HIF1α signaling in normoxia and modulate vascular smooth muscle cell function in pulmonary vascular disease.

This study identifies GLUT1 as a target of SSRIs, showing citalopram inhibits HCC by reversing the Warburg effect through GLUT1 antagonism.

This study investigates metabolic flexibility in hair follicle stem cell-derived squamous cell carcinoma by blocking glycolysis and glutaminolysis, showing tumors can compensate by upregulating lactate consumption.