Cancer, Hypoxia, and Metabolism

This study shows that hepatic stellate cells enhance HCC proliferation through HIF-dependent metabolic changes and H2O2 signaling.

This study identifies SLC25A32 as a critical mitochondrial folate transporter that becomes essential in serine/glycine-starved triple-negative breast cancer, making it a potential therapeutic target.

This study identifies a metabolic tradeoff between fast growth and flexibility in cancer cells and stem cells by analyzing glutamine and aspartate metabolism.

This study identifies Survivin as a critical KRAS signaling partner that promotes glycolytic activity in PDAC cells by forming microtubule-based complexes with glycolytic enzymes.

This study shows that MAGEA3/6 proteins in pancreatic cancer cells enhance metabolic flexibility by regulating glycolysis and mitochondrial metabolism, revealing therapeutic vulnerabilities.

This study shows hypoxia reduces LRIG1 protein levels in colorectal cancer organoids despite increased mRNA, suggesting limitations in LRIG1-based cancer therapies under hypoxic conditions.

This study shows that β-catenin activation in liver cancer cells reduces mitochondrial pyruvate carrier expression and shifts metabolism from carbohydrate to fatty acid oxidation.

The paper defines a Pyruvate Partitioning Index (PPI) to analyze pyruvate metabolism across cell types and tissue space in colorectal cancer, finding it correlates with immune programs and survival.

The paper identifies increased MCT4-associated lactate export in myeloid cells during HNSCC progression using single-cell RNA-sequencing and metabolic flux analysis.

This study shows that ARID1A loss in ovarian clear cell carcinoma maintains increased mitochondrial respiration and bioenergetic efficiency under metabolic challenges, with specific ETC protein changes.

The paper directly measures CO2 and O2 fluxes in anoxic mammalian cells, revealing oxygen-independent decarboxylation that persists after oxygen removal.

This study shows cyclic hypoxia promotes breast cancer growth through WNT5A-ROR1 signaling between stromal and tumor cells in a co-culture model.