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Peng Li and Ming-Qin Wang designed the study; Peng Li, Shao-Ping Tian, Jing Chen and Peng-Hui Song performed the experiments; Peng Li, Shao-Ping Tian, Jing Chen, Peng-Hui Song, and Ming-Qin Wang analyzed the data; Shao-Ping Tian, Jing Chen, and Ming-Qin Wang wrote the manuscript; all authors read and approved the final manuscript.
In addition, we also found that the suppression of COX-2, by which the production of PGE2 is inhibited, could synergistically enhance the anticancer activity of E7050 in MES-SA/Dx5 cells. It has been reported that PGE2 is a potent mitogen with growth-promoting activity in a variety of cell types [37]. Cyclooxygenase 2 (COX-2) is induced by inflammatory cytokines, growth factors, hormones, and mitogens in many cell types and plays a crucial role in the pathogenesis of several human diseases, including cancer [37,38]. COX-2 expression is induced in human breast cancer and its gene expression is commonly upregulated in breast cancer in relation to tumor progression [39]. Moreover, it has been reported that PGE2 could promote the growth of various tumors [40]. Evidence has demonstrated that COX-2 inhibitors or PGE2 receptor antagonists exhibit potent anticancer activities in cancer treatment [41]. Our results showed that COX-2 inhibitor could enhance the inhibition of cell proliferation and apoptosis induced by E7050. Therefore, the combination of COX-2 inhibitor and E7050 may be a promising strategy for the treatment of cancer.
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One of the drawbacks to this approach was that we needed to recompile every time we made even a small change to the code. This slowed everything else we were doing down and because we couldn't always have someone waiting for the application to finish building. 827ec27edc