Effects of Artemin and its receptor GFRα - 3 on the invasion and metastasis of human pancreatic cancer cell line MIA PaCa-2
10.3760/cma.j.issn.1008-1372.2010.10.001
- VernacularTitle:Artemin及受体GFRα3对MIA PaCa-2人胰腺癌细胞浸润和转移能力的影响
- Author:
Zhaojun DING
;
Lingxin MENG
;
Jiangtao LI
;
Shuyan SUN
;
Xiping CHEN
;
Mingde LEI
- Publication Type:Journal Article
- Keywords:
Nerve growth factors/AD;
Receptors,nerve growth factor /AD;
Pancreatic neoplasms/DT;
Neoplasm invasiveness;
Neoplasm metastasis
- From:
Journal of Chinese Physician
2010;12(10):1297-1300
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effects of artemin and its receptor GFRα - 3 on the invasion and metastasis of pancreatic cancer cells. Methods Human pancreatic cancer cell line MIA PaCa -2 was used in this study. Transwell cell culture chamber assay in vitro was used to detect the ability of invasion and metastasis of MIA PaCa -2 cells. The influence of artemin and GFRα -3 on the protein expression of MMP-2 and E-cadherin was investigated by Western blot and quantitative real time polymerase chain reaction-analyses (Q-RT-PCR). Results As the increase of artemin and GFRα -3, the invasion and metastasis of MIA PaCa- 2 was markedly increased [ 150 ng / ml concentration: Artemin group: 107.4 ± 11.4;GFRα3 group:94. 4 ± 9. 3 ;control group:34. 6 ± 7. 3, P < 0. 01 ]. With 150 ng / ml artemin and GFR-3,the synthesis of MMP-2 in MIA PaCa 2 cells was significantly increased than that in control group[ Artemin grou: (2. 17 ± 0. 05 ) × 108; GFRα3 group: (2. 02 ± 0. 03 ) × 108; control group: ( 1.02 ± 0. 02 ) × 108, t =6. 35,7. 32 ], while E-cadherin significantly decreased [ Artemin group: ( 0. 65 ± 0. 04 ) × 108; GFRα3 group: (0. 74 ± 0. 01 ) × 108; control group: ( 1. 36 ± 0. 03 ) × 108, t = 4. 27,5.61 ], the difference was statistically significant ( P <0. 01 ). Conclusions Artemin and its receptor GFRα3 could promote pancreatic cancer cell invasion and metastasis. This effect may be related to the up-regulated expression of MMP-2 and down regulated expression of E-cadherin.
