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Cancer cells utilize large amounts of ATP to sustain growth, relyingprimarily on non-oxidative, fermentative pathways for its production. In manytypes of cancers this leads, even in the presence of oxygen, to the secretionof carbon equivalents (usually in the form of lactate) in the cell'ssurroundings, a feature known as the Warburg effect. While the molecular basisof this phenomenon are still to be elucidated, it is clear that the spilling ofenergy resources contributes to creating a peculiar microenvironment fortumors, possibly characterized by a degree of toxicity. This suggests thatmechanisms for recycling the fermentation products (e.g. a lactate shuttle) maybe active, effectively inducing a mutually beneficial metabolic couplingbetween aberrant and non-aberrant cells. Here we analyze this scenario througha large-scale in silico metabolic model of interacting human cells. By goingbeyond the cell-autonomous description, we show that elementaryphysico-chemical constraints indeed favor the establishment of such a couplingunder very broad conditions. The characterization we obtained by tuning theaberrant cell's demand for ATP, amino-acids and fatty acids and/or theimbalance in nutrient partitioning provides quantitative support to the ideathat synergistic multi-cell effects play a central role in cancer sustainment.

Quantitative constraint-based computational model of tumor-to-stroma coupling via lactate shuttle