Egidio Iorio1, Chiara Alberti2,
Paola Alberti2, Alessandro Ricci1, Maria Elena Pisanu1,
Patrizia Pinciroli2, Silvana Canevari2,
1Cell Biology &
Neurosciences, Istituto Superiore di Sanit, Roma, RM,
Our previous MRS studies showed 3-to-8-fold increases in phosphocholine (PCho) in epithelial ovarian cancer (EOC) cells compared with non tumoral counterparts. The contribution of the PI3K/AKT pathway to PCho accumulation was investigated in three EOC cell lines exposed to the PI3K inhibitor Ly294002. PI3K inhibition was associated with strong decrease in AKT phosphorylation and block of cell proliferation in two LY294002-sensitive (IGROV1 and OAW42) but not in the resistant SKOV3 cells. No alterations were however detected in the PCho levels of any of these cell lines, indicating that multiple pathways likely contribute to the PCho accumulation detected in EOC cells.
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