Inhibiting effects of non-steroidal anti-inflammatory drugs on growth of colon cancer cells in vitro through activator protein-1 and nuclear factor-?? signal transduction pathway
- VernacularTitle:非甾体类抗炎药经转录活化蛋白-1及核因子-?B信号传导通路抑制结肠癌细胞生长
- Author:
Chunhui WANG
;
Qin OUYANG
;
Chengwei TANG
- Publication Type:Journal Article
- Keywords:
Colon cancer;
Cyclooxygenase;
Activator protein;
Nuclear factor
- From:
Chinese Journal of Digestion
2001;0(08):-
- CountryChina
- Language:Chinese
-
Abstract:
Objective To evaluate the inhibiting effect of selective and non-selective cyclo-oxygenase-2(COX-2) inhibitor on growth of colon cancer cell lines in vitro and its signal transduction pathway. Methods The proliferation of colon cancer cells was determined by MTT assay. COX-2, nuclear factor(NF)-?Bp65, extracellular-signal regulated kinase(ERK), phospho ERK(pERK) protein expressed in colon cancer cell lines were analyzed by Western blot. Activator protein(AP)-1 and NF-?B binding activity influenced by non-steroidal anti-inflammatory was detected by electrophoretic mobility sift assay. Results Aspirin and celecoxib could inhibit the proliferation of HT-29, SW480 and LS174-T cells and showed a dose-dependent manner. Western blot analysis showed that expression of COX-2, pERK, NF-?Bp65 protein in colon cancer cells were down-regulated by celecoxib or aspirin in some degree but not effect in total ERK expression. AP-1 and NF-?B binding activity could be stimulated by 20% fetal calf serum or tumor necrosis factor-?. Both aspirin and celecoxib could inhibit fetal calf serum-induced AP-1 activation in HT-29 and SW480 cells. Celecoxib could also inhibit tumor necrosis factor induced NF-?B binding activity, but aspirin had little effects on SW480 cells. Conclusion NSAIDs are able to potentially inhibit the growth of colon cell lines in vitro and the mechanism may relate to AP-1 and NF-?B signal transduction pathway.
