Abstract: Objective 　To investigate the role of p38MAPKin mediating celecoxib (COX-2 selective inhibitor) inhibited the growth of tumor in colon cancer cells and it s relationship COX-2. Methods 　The cell gowth activity of HT-29 cells after the treatment by celecoxib was observed by MTT assay, flow cytometry was used to observed the effect of celecoxib and SB203580 (p38MAPK specific inhibitor ) on apoptosis and the cell cycle dist ribution of HT-29 cells, the expression of Phosph-p38MAPK and COX-2 protein was detected by Western blot . Results 　Compared with the expression of p38MAPK(0. 23 ±0. 12) and COX-2 (0. 95 ±0. 14 ) of control group, p38MAPK expression ( 0. 62 ±0. 11 ) was higher than control group, while the expression of COX-2 (0. 44 ±0. 11) was lower than cont rol group which was treated by celecoxib. SB203580 could decrease the expression of p38MAPK(0. 12 ±0. 05) and COX22 (0. 23 ±0. 13) ;the expression of p38MAPK(0. 43 ±0. 12) was lower than control group, which was between celecoxib and SB203580, the decrease of COX-2 was most significant (0. 15 ±0. 10) . Compared with the apoptosis of cont rol group (4. 31 %), celecoxib and celecoxib + SB203580 induced apoptosis significantly ( P < 0. 01 and P < 0. 05), the apoptosis rate of them was 40. 95 %、26. 24 % respectively. Conclusion 　Celecoxib can induced the apoptosis of human colon cancer HT-29 cell lines, which may through the activation of p38MAPK. In signal t ransduction of HT-29 cell lines, the upst ream kinase of COX-2 is p38MAPK, the expression of COX-2 was regulation by p38MAPK, which has the effect of degenerative feedback regulation by COX-2. Celecoxib induced the apoptosis of tumor cells and play the role of anti-neoplasiasm through COX-2 and p38MAPK.