Escin suppresses migration and invasion involving the alteration of CXCL16/CXCR6 axis in human gastric adenocarcinoma AGS cells.

Abstract

Escin, a natural mixture of triterpene saponins isolated from horse chestnut, has been reported to possess anticancer activity in many human cancer cells. However, the effect of escin on the metastasis has not been studied. The present study examined the effect of escin on the migration and invasion of AGS human gastric cancer cells. To examine the effects of escin on metastatic capacities of gastric cancer cells, AGS cells were cultured in the presence of 0-4 μmol/L escin. Escin inhibited cell migration and invasion in AGS cells. However, escin did not affect the viability of these cells at these concentrations. The chemokine receptor and its ligands play an important role in cancer metastasis. Escin decreased the production of soluble C-X-C motif chemokine (CXCL)16 but increased the expression of trans-membranous CXCL16. The expression of C-X-C chemokine receptor (CXCR)6 was not affected by escin treatment. Exogenous CXCL16 reversed escin-induced migration inhibition. In addition, escin inhibited the phosphorylation of focal adhesion kinase and Akt. These results demonstrate that escin inhibited the migration and invasion of AGS cells, which is associated with altered CXCL16/CXCR6 axis. These findings suggest that escin has potential as an antimetastatic agent in gastric cancer.

• Authors: Hyun Sook Lee, Ji Eun Hong, Eun Ji Kim, Sun Hyo Kim
• Journal: Nutrition and cancer (Nutr Cancer) Vol. 66 Issue 6 Pg. 938-45 ( 2014) ISSN: 1532-7914 [Electronic] United States
• PMID: 24911042 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• CXCL16 protein, human
• CXCR6 protein, human
• Chemokine CXCL16
• Chemokines, CXC
• Receptors, CXCR6
• Receptors, Chemokine
• Receptors, Scavenger
• Receptors, Virus
• Escin
• Focal Adhesion Kinase 1
• PTK2 protein, human
• Proto-Oncogene Proteins c-akt

Topics

• Adenocarcinoma (genetics, pathology)
• Cell Line, Tumor
• Cell Movement (drug effects)
• Cell Survival (drug effects)
• Chemokine CXCL16
• Chemokines, CXC (genetics, metabolism)
• Escin (pharmacology)
• Focal Adhesion Kinase 1 (genetics, metabolism)
• Humans
• Neoplasm Invasiveness
• Phosphorylation
• Proto-Oncogene Proteins c-akt (genetics, metabolism)
• Receptors, CXCR6
• Receptors, Chemokine (genetics, metabolism)
• Receptors, Scavenger (genetics, metabolism)
• Receptors, Virus (genetics, metabolism)
• Signal Transduction
• Stomach Neoplasms (genetics, pathology)