Objective: To investigate possible signal pathway involvement in multi-drug resistant P-glycoprotein (P-gp)expression induced by cyclooxygenase-2 (COX-2) in a human gastric adenocarcinoma cell line stimulated withpacliaxel (TAX). Methods: The effects of TAX on SGC7901 cell growth with different doses was assessed byMTT assay, along with the effects of the COX-2 selective inhibitor NS-398 and the nuclear factor-ΚB (NF-ΚB)pathway inhibitor pyrrolidine dithiocarbamate (PDTC). Influence on COX-2, NF-ΚB p65 and P-gp expressionwas determined by Western blotting. Results: TAX, NS-398 and PDTC all reduced SGC7901 growth, with dosedependence.With increasing dose of TAX, the expression of COX-2, p65 and P-gp showed rising trends, thisbeing reversed by NS-398. PDTC also caused decrease in expression of p65 and P-gp over time. Conclusion:COX-2 may induce the expression of P-gp in SGC7901 cell line via the NF-kappa B pathway with pacliaxelstimulation.
(2012). Mechanism of P-glycoprotein Expression in the SGC7901 Human Gastric Adenocarcinoma Cell Line Induced by Cyclooxygenase-2. Asian Pacific Journal of Cancer Prevention, 13(5), 2379-2383.
MLA
. "Mechanism of P-glycoprotein Expression in the SGC7901 Human Gastric Adenocarcinoma Cell Line Induced by Cyclooxygenase-2". Asian Pacific Journal of Cancer Prevention, 13, 5, 2012, 2379-2383.
HARVARD
(2012). 'Mechanism of P-glycoprotein Expression in the SGC7901 Human Gastric Adenocarcinoma Cell Line Induced by Cyclooxygenase-2', Asian Pacific Journal of Cancer Prevention, 13(5), pp. 2379-2383.
VANCOUVER
Mechanism of P-glycoprotein Expression in the SGC7901 Human Gastric Adenocarcinoma Cell Line Induced by Cyclooxygenase-2. Asian Pacific Journal of Cancer Prevention, 2012; 13(5): 2379-2383.