EpCAM is overexpressed in gastric cancer and its downregulation suppresses proliferation of gastric cancer
- First Online:
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.
KeywordsEpCAM Gastric cancer siRNA Proliferation
- Calabrese G, Crescenzi C, Morizio E et al (2001) Assignment of TACSTD1 (alias TROP1, M4S1) to human chromosome 2p21 and refinement of mapping of TACSTD2 (alias TROP2, M1S1) to human chromosome 1p32 by in situ hybridization. Cytogenet Cell Genet 92:164–165. doi:10.1159/000056891 PubMedCrossRefGoogle Scholar
- Ploverini PJ (1996) Cellular adhesion molecules: newly identified mediators of angiogenesis. Am J Pathol 148:1023–1029Google Scholar