| The objective of this study was to investigate the role of epithelial cell adhesion molecule(EpCAM) in the genesis and the progress of prostate cancer, especially of castration-resistant prostate cancer. Protein expression of EpCAM in 50 pairs of prostate cancer tissues and normal adjacent tissues, plus three cell lines, was examined. Acording to patient follow-up information, high EpCAM expression indicates Short hairpin RNA(shRNA) interference technique was employed to silence the expression of EpCAM in prostate cancer cell LNCaP and construct a stable transfected cell line. In vitro assay was conducted to analyze the effect of EpCAM expression on the expressions of Androgen receptor(AR), Prostate specific antigen(PSA), cell cycle markers and EMT related markers. EpCAM was found significantly expressed higher in prostate cancer tissues than in normal adjacent tissues( P<0.05). In three cell lines(DU-145, PC-3, and LNCaP), the expression of EpCAM in LNCaP, androgen-dependent prostate cancer cells, was significantly higher than that in the other two( P<0.05).As EpCAM was silenced in LNCaP, cell cycle was arrested and cellular abilities of proliferation and invasion were obviously inhibited. Also, the expression levels of AR, PSA and cyclying D, cycling E obviously descended,. EMT related markers were altered as Vimentin and N-cadherin were inhibited and E-cadherin increased. The overexp ression of EpCAM has correlation with the genesis of prostate cancer, especially androgen-dependent prostate cancer. As the expression of AR is facilitated, prostate cancer cells’ abilities to proliferate and invade are consequently enhanced. Our study can provide more theoretical basis to find an promising candidate of the target molecules,in order to the immunotherapy of the prostate cancer. |
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