Abstract
Abnormal accumulation and activation of the recepteur d'origine nantais (RON) has been implicated in carcinogenesis of epithelial tumors. RON expression was induced by the tumor promoter, phorbol 12-myristate 13-acetate (PMA), in gastric adenocarcinoma AGS cells. Studies with deleted and site-directed mutagenesis of Egr-1 promoter and with expression vectors encoding Egr-1 confirmed that Egr-1 is essential for RON expression. In addition, AGS cells pretreated with PMA showed remarkably enhanced invasiveness, which was partially abrogated by siRNA-targeted RON and Egr-1. These results suggest that tumor promoter induces RON expression via Egr-1, which, in turn, stimulates cell invasiveness in AGS cells.
© 2011 Wiley Periodicals, Inc.
Publication types
-
Research Support, Non-U.S. Gov't
MeSH terms
-
Adenocarcinoma / enzymology
-
Adenocarcinoma / metabolism
-
Adenocarcinoma / pathology*
-
Base Sequence
-
Blotting, Western
-
Cell Line, Tumor
-
Chromatin Immunoprecipitation
-
DNA Primers
-
Early Growth Response Protein 1 / genetics
-
Early Growth Response Protein 1 / physiology*
-
Humans
-
Mutagenesis, Site-Directed
-
Neoplasm Invasiveness*
-
Promoter Regions, Genetic
-
RNA, Small Interfering / genetics
-
Receptor Protein-Tyrosine Kinases / metabolism*
-
Reverse Transcriptase Polymerase Chain Reaction
-
Stomach Neoplasms / enzymology
-
Stomach Neoplasms / metabolism
-
Stomach Neoplasms / pathology*
-
Up-Regulation*
Substances
-
DNA Primers
-
EGR1 protein, human
-
Early Growth Response Protein 1
-
RNA, Small Interfering
-
RON protein
-
Receptor Protein-Tyrosine Kinases