Metabolic Remodeling: How Cancer Survives [Oct. 15, 2025] 

Cancer has long been defined by the Warburg effect, yet many tumors also depend on mitochondrial OXPHOS, using both pathways as conditions change. This metabolic plasticity serves as a survival strategy that supports growth and stress tolerance under nutrient and oxygen constraints. To frame this landscape, we introduce a recent review that charts glycolysis, OXPHOS, glutaminolysis, and lipid metabolism in cancer and outlines actionable metabolic targets. We also highlight new research showing that cancers can reprogram the metabolism of neighbouring cells, notably shifting the glycolysis/OXPHOS balance in T cells via mitochondrial transfer and thereby weakening antitumor immunity.

Altered metabolism in cancer: insights into energy pathways and therapeutic targets (Molecular Cancer, 2024)
Summary: Tumor cells undergo metabolic reprogramming, switching between Glycolysis and OXPHOS in response to nutrient and oxygen constraints in the tumor microenvironment to sustain proliferation and stress tolerance.
This review integrates Glycolysis and OXPHOS with glutaminolysis and lipid metabolism in cancer, catalogues actionable targets from glucose transporters, glycolytic enzymes and LDH to electron transport and ATP synthesis, glutaminase, lipid synthesis and fatty-acid oxidation, and emphasizes metabolic plasticity and context-dependent drug sensitivity. Accordingly, analyzing Glycolysis/OXPHOS balance and switching with glucose uptake and lactate production, OCR, and mitochondrial function metrics is essential for revealing plasticity and context-specific vulnerabilities for combination and synthetic-lethal therapy.

 Related techniques  Glycolysis/OXPHOS Assay, Glucose Uptake Plate Assay

Immune evasion through mitochondrial transfer in the tumour microenvironment (Nature, 2025)
Summary: Cancer cells transfer mtDNA-mutant mitochondria to tumor-infiltrating T cells, reprogramming T-cell metabolism and shifting the glycolysis/OXPHOS balance. This mitochondrial transfer drives T-cell dysfunction and senescence, weakening antitumor immunity and pointing to interventions that block mitochondria transfer or modulate mitophagy.

Highlighted technique: In this study, co-cultured cancer cells and T cells, tracked fluorescently labeled mitochondria by confocal, time-lapse, and electron microscopy, and quantified transfer with flow cytometry. 

 Related techniques   Long-lasting Mitochondrial Staining, Mitophagy Detection

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