The inhibition of ibuprofen on the growth of hepatoma carcinoma cell BEL-7402 and the preliminary ;mechanisms
10.3969/j.issn.1007-3969.2015.04.009
- VernacularTitle:布洛芬抑制人肝癌细胞BEL-7402生长及机制的初步研究
- Author:
Ting ZHANG
;
Huiyi WU
;
Huanhuan ZHANG
;
Jin YANG
- Publication Type:Journal Article
- Keywords:
Ibuprofen;
BEL-7402 HCC cell;
Proliferation;
Apoptosis;
PGE2
- From:China Oncology
2015;(4):294-299
- CountryChina
- Language:Chinese
-
Abstract:
Background and purpose:Recently, studies showed that non-steroidal anti-inlfammatory drugs (NSAIDs) could reduce the incidence of cancer. Whether ibuprofen could inhibit the growth of hepatocellular carcinoma cells had not been reported yet. In the current study, we investigated the effects of ibuprofen on hepatoma carcinoma BEL-7402 cells and the relevant mechanisms. Methods: Hepatocellular carcinoma BEL-7402 cells were randomly divided into 7 groups:the control group and the ibuprofen groups (0.1, 0.5, 1.0, 2.0, 3.0 and 4.0 mmol/L). The effect of ibu-profen on BEL-7402 HCC cells was measured by MTT method, the cell cycles were analyzed by flow cytometry (FCM), cell vitality and apoptosis were determined by cell analyzer. PCNA, Cyclin D1, Bcl-2 and COX-2 protein levels were examined by Western blot, and the expressions of prostaglandin E2 (PGE2) were measured by ELISA. Results:After the exposure to ibuprofen, the suppression ratio of BEL-7402 cells was increased (P<0.05). BEL-7402 cell vitality was decreased by degrees significantly (P<0.05), early apoptosis of BEL-7402 cells was increased (P<0.05), and the G0/Gl phase ratio was increased significantly compared with control group (P<0.05). Ibuprofen effectively decreased PCNA, Cyclin D1, Bcl-2 and COX-2 expressions in BEL-7402 cells (P<0.05), and decreased PGE2 protein expression in cell culture supernatants sig-nificantly (P<0.05). Conclusion:Ibuprofen is effective for inhibiting the proliferations, increasing apoptosis and blocking cell cycles of BEL-7402 HCC cells. The anti-tumor mechanisms of ibuprofen may be related with the inhibition of COX-2 and PGE2 expressions.
