Role of PI3K/AKT pathways in mitomycin-mediated apoptosis of WB-F344 cells.
- Author:
Peng YAO
1
;
Dawei YANG
;
Darong HU
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Apoptosis; Blotting, Western; Cell Line; Chromones; Flow Cytometry; Mitomycin; Morpholines; Phosphatidylinositol 3-Kinases; Proto-Oncogene Proteins c-akt; Rats; Signal Transduction; p38 Mitogen-Activated Protein Kinases
- From: Chinese Journal of Hepatology 2015;23(3):200-203
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the role of p38MAPK and PI3K/AKT pathways in mitomycin (MMC)-induced apoptosis in the liver stem-like cell line WB-F344.
METHODSWB-F344 cells were exposed to MMC and apoptosis was evaluated by flow cytometry and DNA fragmentation. Phospho-MAPK and phospho-PI3K/AKT were detected by western blotting.
RESULTSMMC induced apoptosis in WB-F344 cells at 6h after addition of MMC; the maximum level of apoptosis was reached at 24h after MMC exposure. The apoptosis effects of MMC were concentration dependent and inhibited when the PI3K pathway was abolished by the specific inhibitor LY294002, but not inhibited when the p38MAPK pathway was abolished by inhibitor SB203508.
CONCLUSIONApoptosis of WB-F344 cells can be induced by MMC.Although MMC can activate both the PI3K/AKT and p38MAPK pathways, the apoptosis effect of MMC occurs via a PI3K pathway and is not dependent on the p38MAPK pathway.
