Nuclear transcription factor CDX2 inhibits gastric cancer‑cell growth and reverses epithelial‑to‑mesenchymal transition in vitro and in vivo.

The epithelial‑to‑mesenchymal transition (EMT) has been noted as a critical event in the early step of cancer metastasis. Recent studies showed that nuclear transcription factor caudal type homeobox transcription factor 2 (CDX2) is a prognostic factor, which acts as a marker of good outcome in gastric cancer (GC) patients. However, the association between CDX2 expression and EMT has remained to be fully elucidated. The present study reported that forced overexpression of CDX2 in MKN45/CDX2 cells inhibited GC‑cell growth and proliferation, and attenuated migration and invasion in vitro. Furthermore, MKN45/CDX2 cells exhibited a significant upregulation of E‑cadherin protein and a significant downregulation of vimentin protein expression. These results were further supported by in vivo tumorigenicity assays, which showed that CDX2 suppressed gastric tumor xenograft growth and inhibited EMT in nude mice. These results indicated that CDX2 is capable of inhibiting GC‑cell growth and invasion. CDX2 may participate in the process of EMT of GC cells by regulating the expression of the epithelial and mesenchymal proteins E‑cadherin and vimentin.