[Effectiveness of p38MAPK activity during drug resistance against HepG2].
OBJECTIVE
To investigate the effectiveness of p38MAPK activity during drug resistance against HepG2.


METHODS
HepG2/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.


RESULTS
The 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.


CONCLUSIONS
The 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.
Tang
Peng
P
Department of Digestive Diseases, Second Affiliated Hospital, Chongqing Medical University, Chongqing 400010, China.
Chen
Wei-qing
WQ
Shen
Wen-yong
WY
D002453:Cell Cycle; D018432:Drug Resistance, Multiple; D019008:Drug Resistance, Neoplasm; D056945:Hep G2 Cells; D006801:Humans; D010766:Phosphorylation; D048051:p38 Mitogen-Activated Protein Kinases / Q000378:metabolism*
D048051:p38 Mitogen-Activated Protein Kinases