Investigation of the mechanisms of coagulation factor VIIa-induced colon cancer SW620 cell proliferation and migration.
- Author:
Wen-Xia SHI
1
;
Hong ZHOU
;
Na LI
;
Hong-Liang HUANG
;
Bao-Cheng ZHOU
Author Information
- Publication Type:Journal Article
- MeSH: Caspase 7; biosynthesis; genetics; Cell Line, Tumor; Cell Movement; drug effects; Cell Proliferation; drug effects; Colonic Neoplasms; metabolism; pathology; Factor VIIa; pharmacology; Humans; Interleukin-8; biosynthesis; genetics; Oligopeptides; pharmacology; RNA, Messenger; metabolism; Receptor, PAR-2; agonists; Thromboplastin; biosynthesis; genetics; p38 Mitogen-Activated Protein Kinases; metabolism
- From: Chinese Journal of Oncology 2009;31(7):485-489
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the mechanisms that coagulation factor VIIa promotes proliferation and migration of a colon cancer cell line (SW620 cells) in vitro.
METHODSThe expression of interleukin 8 (IL-8), tissue factor (TF), caspase-7 and p-p38 MAPK in SW620 cells treated with factor VIIa or protease activated receptor 2 agonist (PAR2-AP) was measured by ELISA, Western-blotting and QT-PCR.
RESULTSFactor VIIa and PAR2-AP induced IL-8 expression at both mRNA and protein levels, upregulated TF mRNA expression and TF activity, but down-regulated caspase-7 mRNA and p-p38 MAPK levels in SW620 cells. The effects of factor VIIa were not only blocked by anti-TF but also by anti-PAR2 antibodies.
CONCLUSIONFactor VIIa binds to TF on cell surface, forming a complex which activates PAR2, then provoking IL-8 and TF expression, and suppresses caspase-7 expression, thus promotes the tumor cell proliferation and migration. p38 MAPK may negatively regulate this process.
