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

Abstract	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.
Authors	Jian-Feng Zhang, Li-Shuai Qu, Xue-Fen Qian, Bei-Lei Xia, Zhen-Biao Mao, Wei-Chang Chen
Journal	Molecular medicine reports (Mol Med Rep) Vol. 12 Issue 4 Pg. 5231-8 (Oct 2015) ISSN: 1791-3004 [Electronic] Greece
PMID	26238762 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References	Biomarkers, Tumor CDX2 Transcription Factor Homeodomain Proteins Trans-Activators
Topics	Animals Biomarkers, Tumor CDX2 Transcription Factor Cell Line, Tumor Cell Movement Cell Proliferation (genetics) Cell Survival (genetics) Cell Transformation, Neoplastic (genetics, metabolism) Disease Models, Animal Epithelial-Mesenchymal Transition (genetics) Gene Expression Heterografts Homeodomain Proteins (genetics, metabolism) Humans Mice Phenotype Stomach Neoplasms (genetics, metabolism, pathology) Trans-Activators (genetics, metabolism) Tumor Burden (genetics)

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