Abstract
Abstract. Altered choline phospholipid metabolism is a metabolic hallmark of cancer. Malignant transformation of breast can-cer cells results in a switch from high glycerophosphocholine (GPC) and low phosphocholine (PC) to low GPC and high PC.Glycerophosphocholine phosphodiesterase (GPC-PDE; E.C. 3.1.4.2) catalyzes the degradation of GPC to choline (Cho) andglycerol-3-phosphate. The GPC-PDE gene(s) responsible for the relatively low GPC concentration in breast cancer cells havenot yet been characterized. Glycerophosphodiester phosphodiesterase domain containing 5 (GDPD5) displays GPC-PDE ac-tivity, and is rapidly inhibited by sodium chloride and urea (NaCl/urea). We chemically inhibited GPC-PDE with NaCl/ureain nonmalignant MCF-12A breast epithelial cells, as well as in MCF-7 and MDA-MB-231 breast cancer cells. 1 H magneticresonance spectroscopy (MRS) of cell extracts demonstrated that exposure of MCF-12A, MCF-7 and MDA-MB-231 cells toNaCl/urea ( n = 5) significantly increased GPC and decreased PC, resulting in a low [PC]
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