Abstract
Extracellular signal-regulated kinase (ERK) activation has been implicated in cell motility and invasion. In this study, we demonstrated that the steady-state levels of activated ERK1/2 correlated with the degree of invasiveness and metastatic potential of three Dunning cancer cell lines, originating from the same parental tumor. Inhibition of mitogen-activated protein kinase kinase 1 (MEK1), an upstream regulator of ERK1/2, with PD98059 resulted in a dose-dependent reduction of invasiveness with different IC50 values in the three Dunning cell lines. These results suggest that ERK is, at least in part, responsible for regulating invasiveness and may underlie the differences in the metastatic ability of the cell lines.
Publication types
-
Research Support, Non-U.S. Gov't
MeSH terms
-
Adenocarcinoma / drug therapy
-
Adenocarcinoma / enzymology*
-
Adenocarcinoma / secondary*
-
Animals
-
Cell Division / drug effects
-
Cell Division / physiology
-
Cell Survival / drug effects
-
Cell Survival / physiology
-
Dose-Response Relationship, Drug
-
Growth Inhibitors / pharmacology
-
Growth Inhibitors / therapeutic use
-
Male
-
Mitogen-Activated Protein Kinase 1 / antagonists & inhibitors
-
Mitogen-Activated Protein Kinase 1 / physiology*
-
Mitogen-Activated Protein Kinase 3
-
Mitogen-Activated Protein Kinases / antagonists & inhibitors
-
Mitogen-Activated Protein Kinases / physiology*
-
Prostatic Neoplasms / drug therapy
-
Prostatic Neoplasms / enzymology*
-
Rats
-
Tumor Cells, Cultured
Substances
-
Growth Inhibitors
-
Mitogen-Activated Protein Kinase 1
-
Mitogen-Activated Protein Kinase 3
-
Mitogen-Activated Protein Kinases