Study of MK promoting breast cancer cell MDA-MB-231 angiogenesis through EPCR/PAR1 pathway in vitro
10.13315/j.cnki.cjcep.2015.09.001
- VernacularTitle:MK 通过 EPCR/PAR1通路促进乳腺癌 MDA-MB-231细胞体外血管生成
- Author:
Qingling WANG
;
Dongmei LIU
;
Zhengjie HAN
;
Yongping WU
- Publication Type:Journal Article
- Keywords:
breast neoplasm;
midkine;
EPCR;
PAR1;
angiogenesis
- From:
Chinese Journal of Clinical and Experimental Pathology
2015;(9):961-965
- CountryChina
- Language:Chinese
-
Abstract:
Purpose To observe the effects of midkine ( MK) on human breast cancer cell line MDA-MB-231 angiogenesis in vitro, and to explore its mechanism. Method shRNA interference was performed to silence the expression of MK in MDA-MB-231 cells, and Western blot was used to identify the expression of MK and EPCR. After MK and EPCR knockdown, or treated with anti protease-activated receptor 1 (PAR1) antibody, the culture medium of MDA-MB-231 cells were collected and the conditioned medium were pre-pared. Human umbilical vein endothelial cells ( HUVECs) were cultured with conditioned medium, and the endothelial cells prolifera-tion was detected by CCK-8 assay, cell migration was detected by transwell method, vasculogenic activity was assessed by Matrigel-based tube formation assay. Results After knockdown of MK, the protein level of EPCR was decreased in MDA-MB-231 cells. Com-pared with control, knockdown of MK and EPCR decreased the proliferation, migration and angiogenesis ability of HUVECs significant-ly (P<0. 05), and the effect of EPCR knockdown group was stronger than MK knockdown group (P<0. 05). After treated with anti-PAR1 antibody, the proliferation, migration and angiogenesis ability of HUVECs were decreased compared with control and EPCR knockdown group (P<0. 05). Conclusion MK promotes human breast cancer cell line MDA-MB-231 angiogenesis through EPCR /PAR1 signaling pathway in vitro.
