Overexpression of phospholipase D suppresses taxotere-induced cell death in stomach cancer cells.

摘要: Phospholipase D (PLD) catalyzes the hydrolysis of phosphatidylcholine to generate phosphatidic acid (PA) and choline. There are at least two PLD isozymes, PLD1 PLD2. Genetic pharmacological approaches implicate both isozymes in a diverse range cellular processes, including receptor signaling, membrane transport control, actin cytoskeleton reorganization. Several recent studies reported that has role signaling pathways oppose apoptosis promote cell survival cancer. In this study, we examined taxotere-induced stomach lines; normal (NSC) cancer cells (SNU 484). Taxotere treatment resulted increase activity. To confirm apoptosis, PLDs were transfected into SNU 484 cells. Overexpression inhibition apoptotic death, evidenced by decreased degradation chromosomal DNA, increased viability. Concurrently, Bcl-2 expression was upregulated, activation procaspase 3 inhibited after PLD's transfection. However, when selectively specific siRNA-PLD1 or -PLD2, exacerbated On top this, PA -- product PLDs, also upregulation 484. Although PA-induced blocked mepacrine, an inhibitor phospholipase A(2) (PLA(2)), not abrogated propranolol, phospholyhydrolase (PAP). Taken together, PLD2 closely related with together PLA(2), but PAP, during