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Article

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

  • Authors:
    • Jian‑Feng Zhang
    • Li‑Shuai Qu
    • Xue‑Fen Qian
    • Bei‑Lei Xia
    • Zhen‑Biao Mao
    • Wei‑Chang Chen
  • View Affiliations / Copyright

    Affiliations: Department of Gastroenterology, The First Affiliated Hospital of Soochow University, Suzhou, Jiangsu 215006, P.R. China, Department of Gastroenterology, Affiliated Hospital of Nantong University, Nantong, Jiangsu 226001, P.R. China
  • Pages: 5231-5238
    |
    Published online on: July 22, 2015
       https://doi.org/10.3892/mmr.2015.4114
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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.
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Copy and paste a formatted citation
Spandidos Publications style
Zhang JF, Qu LS, Qian XF, Xia BL, Mao ZB and Chen WC: Nuclear transcription factor CDX2 inhibits gastric cancer‑cell growth and reverses epithelial‑to‑mesenchymal transition in vitro and in vivo. Mol Med Rep 12: 5231-5238, 2015.
APA
Zhang, J., Qu, L., Qian, X., Xia, B., Mao, Z., & Chen, W. (2015). Nuclear transcription factor CDX2 inhibits gastric cancer‑cell growth and reverses epithelial‑to‑mesenchymal transition in vitro and in vivo. Molecular Medicine Reports, 12, 5231-5238. https://doi.org/10.3892/mmr.2015.4114
MLA
Zhang, J., Qu, L., Qian, X., Xia, B., Mao, Z., Chen, W."Nuclear transcription factor CDX2 inhibits gastric cancer‑cell growth and reverses epithelial‑to‑mesenchymal transition in vitro and in vivo". Molecular Medicine Reports 12.4 (2015): 5231-5238.
Chicago
Zhang, J., Qu, L., Qian, X., Xia, B., Mao, Z., Chen, W."Nuclear transcription factor CDX2 inhibits gastric cancer‑cell growth and reverses epithelial‑to‑mesenchymal transition in vitro and in vivo". Molecular Medicine Reports 12, no. 4 (2015): 5231-5238. https://doi.org/10.3892/mmr.2015.4114
Copy and paste a formatted citation
x
Spandidos Publications style
Zhang JF, Qu LS, Qian XF, Xia BL, Mao ZB and Chen WC: Nuclear transcription factor CDX2 inhibits gastric cancer‑cell growth and reverses epithelial‑to‑mesenchymal transition in vitro and in vivo. Mol Med Rep 12: 5231-5238, 2015.
APA
Zhang, J., Qu, L., Qian, X., Xia, B., Mao, Z., & Chen, W. (2015). Nuclear transcription factor CDX2 inhibits gastric cancer‑cell growth and reverses epithelial‑to‑mesenchymal transition in vitro and in vivo. Molecular Medicine Reports, 12, 5231-5238. https://doi.org/10.3892/mmr.2015.4114
MLA
Zhang, J., Qu, L., Qian, X., Xia, B., Mao, Z., Chen, W."Nuclear transcription factor CDX2 inhibits gastric cancer‑cell growth and reverses epithelial‑to‑mesenchymal transition in vitro and in vivo". Molecular Medicine Reports 12.4 (2015): 5231-5238.
Chicago
Zhang, J., Qu, L., Qian, X., Xia, B., Mao, Z., Chen, W."Nuclear transcription factor CDX2 inhibits gastric cancer‑cell growth and reverses epithelial‑to‑mesenchymal transition in vitro and in vivo". Molecular Medicine Reports 12, no. 4 (2015): 5231-5238. https://doi.org/10.3892/mmr.2015.4114
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