Abstract
To identify the role of epithelial cellular adhesion molecule (EpCAM) in gastric cancer growth and explore the potential value of EpCAM monoclonal antibody as new therapeutic strategy for gastric cancer. The expression of EpCAM was determined by immunohistochemistry staining in gastric cancer tissues, RT-PCR and Western blot in cell lines. EpCAM expression in cell lines was downregulated by small interfering RNA. Then the effects of EpCAM on gastric cancer cell growth in vivo and in vitro were determined by MTT, FCM analysis, clone formation assay and tumor formation assay. Additionally, western blot was used to detect the effect of EpCAM on cell cycle-relevant factor cyclin D1. EpCAM was found to be overexpressed in gastric cancer tissues and cell lines. Downregulation of EpCAM resulted in a decrease of cell proliferation and cell cycle arrest in AGS and SGC7901 cells, which had high endogenous EpCAM expression. EpCAM downregulation also suppressed tumor formation in nude mice. Moreover, EpCAM repression in gastric cancer cells could downregulate cyclin D1. EpCAM was a potential oncogene and contributed to the growth of gastric cancer. Our data first provided compelling evidence of potential value of EpCAM in the therapy of gastric cancer in clinic.
Published Version
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