Investigation of the signal transduction in EG- VEGF inhibiting pancreatic cancer cells from apoptosis
10.3760/cma.j.issn.1674-1935.2011.03.015
- VernacularTitle:内分泌腺来源的血管内皮生长因子抑制胰腺癌细胞凋亡的信号转导机制研究
- Author:
Linan REN
;
Xiaozhong GUO
;
Deli ZOU
;
Feng LIU
- Publication Type:Journal Article
- Keywords:
Pancreatic neoplasm;
Vascular endothelial growth factor;
Apoptosis;
Signal transduction
- From:
Chinese Journal of Pancreatology
2011;11(3):194-196
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the anti-apoptosis effects of EG-VEGF on pancreatic cancer cell MiaPaCa and its molecular mechanism. Methods The cells were treated with 50, 100, 200 ng/ml EG-VEGF. Flow cytometry was used to determine the apoptosis. The expression of p42/44MAPK, STAT3 protein and the phosphorylation, and anti-apoptosis protein Mcl-1 was evaluated by Western blot. Non-specific G protein-coupled receptor antagonist PTX, Rsa/ERK signal transduction blockade PD98059, JAK/STAT3 signal transduction blockade AG490 were used to treat the cells for 1 h, and the change of Mcl-1 protein was observed. Results After treated with 50 ng/ml EG-VEGF, the apoptosis rate of MiaPaCa was decreased from (28.4 ±4.6)% to (13.21 ±4.65)% (P<0.05) ; the phosphorylation of p42/44MAPK increased by 1.735 ± 0.019 folds; the phosphorylation of STAT3 increased by 21.810 ± 0.052 folds; the expression of Mcl-1 protein increased by 3.460 ±0.002 folds when compared with that of control group,and the difference was statistically significant (P < 0.05 ). But the degree of phosphorylation and the expression of Mcl-1 were not further increased with 100, 200 ng/ml EG VEGF treatment. After PTX pre-treatment, the increase of Mcl-1 protein expression was completely inhibited, and after PD98059, AG490 pre-treatment, the increase of Mcl-1 expression was inhibited to 52% and 68%. Conclusions EG-VEGF can inhibit MiaPaCa cell from apoptosis,and the mechanism may be related with activation of Ras MAPK and JAK STAT3 signal transduction pathway and up-regulation of Mcl-1.
