Abstract
In order to prove whether downregulation of COX-2 (Cyclooxygenase-2) could modulate the epithelial- mesenchymal transition (EMT) of breast cancer, celecoxib and siRNA were respectively used to inhibit COX-2 function and expression in MDA-MB-231 cells. The EMT reversal effect in the RNAi treated group was better than that of the celecoxib group while there were no obvious differences in the medium PGE2 levels between the two groups. The results show that COX-2 pathways may contribute considerably to EMT of breast cancer cells, partially dependent on the PGE2 cascade. Akt2, ZEB2 and Snail were measured to clarify the underlying mechanisms of COX-2 on EMT; COX-2 may modulate EMT of breast cancer by regulating these factors. This finding may be helpful to elucidate the mechanisms of selective COX-2 inhibitor action in EMT modulation in breast cancer.
Highlights
Cyclooxygenase (COX) is the rate-limiting enzyme that regulates the synthesis of prostaglandins and thromboxanes from free arachidonic acid (Williams et al, 1999)
The results show that COX-2 pathways may contribute considerably to epithelialmesenchymal transition (EMT) of breast cancer cells, partially dependent on the PGE2 cascade
A series of phenotypic and molecular changes occur in cancer cells during EMT, and leads to adverse prognosis (Thompson et al, 2005; Kalluri and Weinberg, 2009), EMT is often associated with a poor prognosis in women with breast cancer (Moody et al, 2005; Ansieau, 2013; Roxanis, 2013)
Summary
Cyclooxygenase (COX) is the rate-limiting enzyme that regulates the synthesis of prostaglandins and thromboxanes from free arachidonic acid (Williams et al, 1999). A series of phenotypic and molecular changes occur in cancer cells during EMT, and leads to adverse prognosis (Thompson et al, 2005; Kalluri and Weinberg, 2009), EMT is often associated with a poor prognosis in women with breast cancer (Moody et al, 2005; Ansieau, 2013; Roxanis, 2013). Due to both overexpression of COX-2 and EMT are correlated directly with highly aggressive and metastatic breast cancer, so there may have close relationship between them (Ogunwobi et al, 2012). Akt is a well-known key pathway for many basic cellular processes, including cell cycle progression, cell proliferation, cell survival, metabolism and EMT For this reason, we concentrate on the regulation of COX-2 on the activation and expression of AKT
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