Sensitization of human glioma SWO cell line to tumor necrosis factor-induced apoptosis by blocking phospholipase C-gamma1 signaling pathway.
- Author:
Jun LIN
1
;
Jin-Cheng YANG
;
Li TAN
;
Shen-Qiu LUO
Author Information
- Publication Type:Journal Article
- MeSH: Apoptosis; drug effects; Blotting, Western; Caspase 3; metabolism; Cell Line, Tumor; Cell Proliferation; drug effects; Cell Survival; drug effects; Dose-Response Relationship, Drug; Down-Regulation; drug effects; Estrenes; pharmacology; Flow Cytometry; Glioma; enzymology; pathology; Humans; Phosphodiesterase Inhibitors; pharmacology; Phospholipase C gamma; antagonists & inhibitors; metabolism; Proto-Oncogene Proteins c-bcl-2; metabolism; Pyrrolidinones; pharmacology; Signal Transduction; drug effects; Tumor Necrosis Factor-alpha; pharmacology
- From: Journal of Southern Medical University 2006;26(3):266-269
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo explore the role of phospholipase C-gamma1 (PLC-gamma1) in tumor necrosis factor-alpha (TNF-alpha)-induced apoptosis of human glioma SWO cells.
METHODSThe PLC-gamma1 pathway was blocked by U73122 in SWO cells, and the inhibitory effect of TNF-alpha on SWO glioma cell proliferation with or without U73122 treatment was investigated by MTT assay. The cell apoptosis induced by TNF-alpha along or in combination with U73122 was detected by flow cytometry with PI staining. The expression of caspase-3 and Bcl-2 was detected by Western blotting.
RESULTS AND CONCLUSIONU73122 can sensitize SWO glioma cells to TNF-alpha-induced apoptosis. Blocking the PLC-gamma1 pathway may not induce apoptosis of SWO glioma cells, but can sensitize SWO glioma cells to small-dose TNF-alpha-induced apoptosis, the mechanism of which may involve down-regulation of bcl-2.
