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Differentiated embryonic chondrocyte (DEC) genes have been reported to be involved in the regulation of mammalian circadian rhythms, differentiation, apoptosis, the response to hypoxia and epithelial‑mesenchymal transition (EMT). Activation of transforming growth factor (TGF)‑β signaling is known to promote EMT for the development of metastatic castration‑resistant prostate cancer (PCa). However, the role of DEC genes in the TGF‑β‑induced EMT of PCa remains unclear. In the present study it was demonstrated that TGF‑β increased the transcriptional/translational levels of DEC1 but decreased those of DEC2 in PC‑3 cells. Moreover, TGF‑β evoked the phosphorylation of Smad2, followed by the activation of mesenchymal markers, such as N‑cadherin and vimentin, in addition to the suppression of epithelial markers, such as E‑cadherin. The knockdown of DEC1 restrained TGF‑β‑induced cell morphology changes as well as cell motility, which was compatible with the upregulation of E‑cadherin and downregulation of pSmad2, N‑cadherin, and vimentin. However, DEC2 knockdown endorsed PC‑3 cells with a more metastatic phenotype. EMT‑related markers in DEC2 siRNA‑transfected cells exhibited a reverse expression pattern when compared with that in DEC1 siRNA‑transfected cells. Taken together, these results provide evidence that DEC1 and DEC2 have opposite effects on TGF‑β‑induced EMT in human prostate cancer PC‑3 cells.

Correlation between DEC1/DEC2 and epithelial‑mesenchymal transition in human prostate cancer PC‑3 cells