Abstract
Aberrant overexpression of autocrine motility factor and its receptor (AMFR) is observed in many cancers but not in esophageal squamous cell cancer (ESCC). In this study, upregulated rho-associated protein kinase 2, p-cofilin and intracellular adhesion molecule-1, and downregulated E-cadherin were found in ESCC cells transfected with the plasmid pcDNA 3.1-AMFR-C, while opposite results were observed in ESCC cells transfected with siRNA against AMFR. Additionally, an elevated invasion of ESCC cells by AMFR was reversed by rho-associated protein kinase 2 inhibitor Y-27632, suggesting that AMFR pathway promotes invasion of ESCC cells and may be a potential target for ESCC therapy.
Publication types
-
Research Support, Non-U.S. Gov't
MeSH terms
-
Blotting, Western
-
Carcinoma, Squamous Cell / metabolism*
-
Carcinoma, Squamous Cell / pathology
-
Enzyme Activation / physiology
-
Esophageal Neoplasms / metabolism*
-
Esophageal Neoplasms / pathology
-
Fluorescent Antibody Technique
-
Humans
-
Neoplasm Invasiveness / pathology
-
Receptors, Autocrine Motility Factor
-
Receptors, Cytokine / metabolism*
-
Reverse Transcriptase Polymerase Chain Reaction
-
Signal Transduction / physiology*
-
Transfection
-
Ubiquitin-Protein Ligases / metabolism*
-
rho-Associated Kinases / metabolism*
Substances
-
Receptors, Cytokine
-
AMFR protein, human
-
Receptors, Autocrine Motility Factor
-
Ubiquitin-Protein Ligases
-
ROCK2 protein, human
-
rho-Associated Kinases