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c‐Met inhibition is required for the celecoxib‐attenuated stemness property of human colorectal cancer cells

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Journal of Cellular Physiology

Published online on


--- - |2- This is the first report that elucidates the mechanism underlying celecoxib‐inhibited cancer stem cell (CSC). c‐Met is identified as a critical factor for the CSC property of colorectal cancer cells. Abstract Cyclooxygenase‐2 (COX‐2) is frequently overexpressed and enhances colorectal cancer (CRC) tumorigenesis, including cancer stem cell (CSC) regulation. Accordingly, nonsteroidal anti‐inflammatory drugs (NSAIDs), inhibiting COX‐1/2 activity, are viewed as potential drugs for CRC treatment. Accumulated evidence indicates that celecoxib has the most potency for antitumor growth among NSAIDs and the underlying mechanism is only partly dependent on COX‐2 inhibition. However, the potency of these NSAIDs on CSC inhibition is still not known. In this study, we found that among these NSAIDs, celecoxib has the most potency for CSC inhibition of CRC cells, largely correlating to inhibition of c‐Met, not COX‐2. Further analysis reveals that c‐Met activity was required for basal CSC property. Silence of c‐Met blocked whereas overexpression of c‐Met enhanced the celecoxib‐inhibited CSC property. Collectively, these results not only first elucidate the mechanism underlying celecoxib‐inhibited CSC but also indicate c‐Met as a critical factor for the CSC property of CRC cells. - 'Journal of Cellular Physiology, EarlyView. '