Phosphomonoester metabolism as a function of cell proliferative status and exogenous precursors.

Elevations of phosphomonoesters (PMEs) correlate with increased cell growth or increased cell degradation, and have been shown to occur in human tumors as well as animal tumor models and cell lines. Furthermore, decreased PME levels have been observed in tumor patients who respond to therapy. Therefore, understanding the mechanisms underlying the interactions of intrinsic and extrinsic control of PMEs may assist diagnosis and treatment of tumors at the clinical level. In order to probe the underlying mechanisms controlling PME concentrations, we used cells grown in bioreactors and 31P nuclear magnetic resonance spectroscopy to study the effects of proliferative status and exogenous precursor amines on the PMEs phosphorylcholine (PCho) and phosphorylethanolamine (PEtn). In general, PEtn demonstrated an inverse correlation with cell growth, beginning to rise as the stationary growth phase was approached. PCho, on the other hand, generally decreased during log growth, an effect that was reversed by the addition of exogenous choline. The net effect of these changes was a consistent and dramatically lower PCho/PEtn ratio in stationary cultures compared to actively proliferating cultures.