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.
Highlights
There is growing interest in understanding the mechanisms regulating the antiproliferative effects of non-steroidal anti-inflammatory drugs (NSAIDs)
The extent of wound closure was correlated with the concentration of indomethacin. These results indicated that indomethacin can inhibit cancer cell migration
We further investigated the effects of indomethacin on endothelial growth factor (EGF)-medicated store-operated Ca2+ influx
Summary
There is growing interest in understanding the mechanisms regulating the antiproliferative effects of non-steroidal anti-inflammatory drugs (NSAIDs). Studies obtained from in vitro experiments indicate that NSAIDs can block cell proliferation, resulting in inhibition of cell growth [1,2]. Indomethacin, one of the most common NSAIDs, possesses anti-inflammatory, analgesic, and antipyretic properties by non-selectively inhibiting both cyclooxygenase (COX)-1 and COX-2 [3]. NSAIDs inhibit synthesis of prostaglandins from arachidonic acid by the COX enzymes [5]. COX-1 is constitutively expressed and is required for physiological processes such as maintenance of the gastrointestinal mucosa and vascular homeostasis, whereas COX-2 is an inducible enzyme that has been linked to inflammatory reactions and cytokine release [6]. The COX-2 gene is overexpressed in human colon cancer, and the high level of COX-2 expression is correlated with mutagenesis and angiogenesis [7]
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