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Effects of COX-2 inhibitor on growth of human gastric cancer cells and its relation to hepatocyte growth factor.

Abstract：

:It is known that hepatocyte growth factor binding to its receptor regulates gastric cancer progression and metastasis. HGF was found to up-regulate the expression of cyclooxygenase-2 gene and increases prostaglandin (PG) synthesis in gastric mucosa cells. Overexpression of COX-2 and increased PG secretion have also been found to be involved in the regulation of growth and metastasis of gastric cancer. Results from this study showed that c-Met and COX-2 are expressed in 28 cases (93.3%) and 16 cases (53.3%) of 30 human gastric cancer tissues, respectively. Expressions of c-Met positively correlated with that of COX-2 (r=0.41; P=0.024). Using in vivo and in vitro models to further examine the interaction between c-MET and COX-2, we found that HGF stimulated the growth of SC-M1 cells in a dose-dependent manner. COX-2-specific inhibitor-NS398 inhibited the growth of human gastric cancer SC-M1 cells as well as HGF stimulated the growth of SC-M1 cells in a dose-dependent manner. HGF treatment of SC-M1 cells increased the secretion of PGE2 and this stimulation was blocked by NS398. In vivo SC-M1 tumor model showed that HGF stimulated the tumor growth and NS398 retarded the tumor growth. These results suggest that COX-2-specific inhibitors may play some role on the therapy of gastric cancer patients with high serum HGF level and overexpression of c-Met in tumor.

journal_name

Cancer Lett

journal_title

Cancer letters

authors

Chen JH,Wu CW,Kao HL,Chang HM,Li AF,Liu TY,Chi CW

doi

10.1016/j.canlet.2005.08.026

keywords:

subject

Has Abstract

pub_date

2006-08-08 00:00:00

pages

263-70

issue

2

eissn

0304-3835

issn

1872-7980

pii

S0304-3835(05)00816-5

journal_volume

239

pub_type

杂志文章

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