Indomethacin inhibits cancer cell migration via attenuation of cellular calcium mobilization

• Published in: Molecules (Basel, Switzerland) Vol. 18; no. 6; pp. 6584 - 6596
• Main Authors: Guo, Yuh-Cherng, Chang, Che-Mai, Hsu, Wen-Li, Chiu, Siou-Jin, Tsai, Yao-Ting, Chou, Yii-Her, Hou, Ming-Feng, Wang, Jaw-Yan, Lee, Mei-Hsien, Tsai, Ke-Li, Chang, Wei-Chiao
• Format: Journal Article
• Language: English
• Published: Switzerland MDPI AG 04.06.2013; MDPI
• Subjects: Anti-inflammatory agents; Anti-Inflammatory Agents, Non-Steroidal - chemistry; Anti-Inflammatory Agents, Non-Steroidal - pharmacology; Calcium - metabolism; Calcium Signaling; Cell adhesion & migration; Cell growth; Cell Line, Tumor; cell migration; Cell Movement - drug effects; Colorectal cancer; COX-2; Cyclooxygenase 2 - genetics; Cyclooxygenase 2 - metabolism; Drug dosages; EGF; Epidermal Growth Factor - pharmacology; ErbB Receptors - metabolism; Gene expression; Gene Expression Regulation, Neoplastic - drug effects; Humans; indomethacin; Indomethacin - chemistry; Indomethacin - pharmacology; Medicine; Neoplasms - genetics; Neoplasms - metabolism; Pharmacy; Phosphorylation - drug effects; Protein expression; Proteins; Wound healing; Taiwan
• ISSN: 1420-3049; 1420-3049
• DOI: 10.3390/molecules18066584

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.