Dipalmitoleoyl-phosphatidylethanolamine induces apoptosis of NCI-H28 malignant mesothelioma cells.
Λέξεις-κλειδιά
Αφηρημένη
OBJECTIVE
The phospholipid phosphatidylethanolamine regulates a wide range of cellular processes. The present study investigated the antitumor effect of 1,2-dipalmitoleoyl-sn-glycero-3-phosphoethanolamine (DPPE) on malignant pleural mesothelioma cells.
METHODS
Activities of protein phosphatases (PPs) such as PP1, PP2A, and protein tyrosine phosphatase 1B (PTP1B) were assayed under cell-free conditions. 3-(4,5-Dimethyl-2-thiazolyl)-2,5-diphenyl-2H-tetrazolium bromide (MTT) assay, terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) staining, and western blotting were carried out on the human Met5A non-malignant mesothelial cell line and NCI-H28 malignant mesothelioma cell line.
RESULTS
DPPE significantly enhanced PP2A and PTP1B activities. DPPE tended to attenuate activity of extracellular signal-regulated kinase-1 (ERK1)/ERK2, with the greater efficacy for NCI-H28 cells than that for Met5A cells. DPPE reduced NCI-H28 cell viability in a concentration (1-100 μM)-dependent manner, while it had no effect on Met5A cell viability. DPPE markedly increased TUNEL-positive cells in the NCI-H28 cell line, but otherwise induced few TUNEL-positive cells in the Met5A cell line.
CONCLUSIONS
The results of the present study clearly demonstrate that DPPE induces apoptosis of NCI-H28 malignant pleural mesothelioma cells. DPPE-induced enhancement of PP2A and PTP1B activities might at least in part contribute to the apoptotic effect of DPPE.
