Effectiveness of p38MAPK activity during drug resistance against HepG2.
- Author:
Peng TANG
1
;
Wei-qing CHEN
;
Wen-yong SHEN
Author Information
- Publication Type:Journal Article
- MeSH: Cell Cycle; Drug Resistance, Multiple; Drug Resistance, Neoplasm; Hep G2 Cells; Humans; Phosphorylation; p38 Mitogen-Activated Protein Kinases; metabolism
- From: Chinese Journal of Hepatology 2010;18(8):604-608
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the effectiveness of p38MAPK activity during drug resistance against HepG2.
METHODSHepG2/CDDP kinetic anti-cancer drug resistance model was constructed using anti-cancer drug inducing method and treated with P38MAPK inhibitor SB203580 for 24, 48 and 72 hours respectively. Flow cytometry (FCM) was used to detect the cell cycle distribution. The IC50 of cisplatin was determined by MTT method in vitro. The expressions of P-P38, P-gp, Bcl-2 and Bax were examined by Western blot.
RESULTSThe HepG2/CDDP kinetic drug resistance model was successfully established. The expression of P-P38 increased with the increasing drug resistance against HepG2 cells. The models treated with SB203580 could gradually elevate the sensitivity of HepG2/CDDP to cisplatin, block the detention of cell cycle, up-regulate the expression of Bax and down-regulate the expressions of Bcl-2 and P-gp.
CONCLUSIONThe expression of P-P38 increased with the increasing drug resistance against hepatocellular carcinoma cells. Suppressing the activation of P38 could reverse the drug resistance phenotype against hepatocellular carcinoma cells.
