Abstract
Aim:We have previously reported that quercetin (Qu) regulates epithelial–mesenchymal transition (EMT) by modulating Wnt signaling components. In this study, we investigated the synergistic effect of Qu and 2-methoxyestradiol (2-ME) and the role of Wnt signaling components in regulating EMT in PC-3 cells.Materials & methods:EMT was induced by treating PC-3 cells with TGF-β, followed by evaluation of expression of EMT markers and Wnt signaling proteins in naive, induced and after exposing induced cells to Qu and 2-ME at both gene and protein level by real-time PCR (RT-PCR) and western blot, respectively.Results:Qu and 2-ME synergistically downregulated mesenchymal markers with simultaneous upregulation of epithelial markers. Wnt signaling proteins expression was also downregulated by Qu and 2-ME in TGF-β-induced EMT in PC-3 cells.Conclusion:Thus, combination therapy of Qu and 2-ME could be a new promising therapeutic approach for the treatment of prostate cancer.
Highlights
Further experimental studies are required to unravel the exact mechanism of action to confirm the possibility of using these two anticancer drugs to treat prostate cancer (PCa)
In this work, we demonstrated that a combination of quercetin (Qu) and 2-methoxyestradiol (2-Me) could inhibit epithelial–mesenchymal transition in prostate cancer (PCa) cells
Wnt signaling pathway is identified as the key molecular player in driving the antitumorigenic effects of the combination of Qu and 2-Me in PCa
Summary
We have previously reported that quercetin (Qu) regulates epithelial–mesenchymal transition (EMT) by modulating Wnt signaling components
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