Abstract
Non-steroidal anti-inflammatory drugs (NSAIDs) were shown to reduce the risk of colorectal cancer recurrence and are widely used to modulate inflammatory responses. Indomethacin is an NSAID. Herein, we reported that indomethacin can suppress cancer cell migration through its influence on the focal complexes formation. Furthermore, endothelial growth factor (EGF)-mediated Ca2+ influx was attenuated by indomethacin in a dose dependent manner. Our results identified a new mechanism of action for indomethacin: inhibition of calcium influx that is a key determinant of cancer cell migration.
Publication types
-
Research Support, Non-U.S. Gov't
MeSH terms
-
Anti-Inflammatory Agents, Non-Steroidal / chemistry
-
Anti-Inflammatory Agents, Non-Steroidal / pharmacology
-
Calcium / metabolism*
-
Calcium Signaling
-
Cell Line, Tumor
-
Cell Movement / drug effects*
-
Cyclooxygenase 2 / genetics
-
Cyclooxygenase 2 / metabolism
-
Epidermal Growth Factor / pharmacology
-
ErbB Receptors / metabolism
-
Gene Expression Regulation, Neoplastic / drug effects
-
Humans
-
Indomethacin / chemistry
-
Indomethacin / pharmacology*
-
Neoplasms / genetics
-
Neoplasms / metabolism*
-
Phosphorylation / drug effects
Substances
-
Anti-Inflammatory Agents, Non-Steroidal
-
Epidermal Growth Factor
-
Cyclooxygenase 2
-
ErbB Receptors
-
Calcium
-
Indomethacin