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. 2012 Jun;39(6):6707-14.
doi: 10.1007/s11033-012-1494-2. Epub 2012 Feb 7.

Loss of E-cadherin promotes the growth, invasion and drug resistance of colorectal cancer cells and is associated with liver metastasis

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Loss of E-cadherin promotes the growth, invasion and drug resistance of colorectal cancer cells and is associated with liver metastasis

Xiaobing Chen et al. Mol Biol Rep. 2012 Jun.

Abstract

The recent studies indicated that the epithelial cell adhesion molecule E-cadherin is a well-recognized molecule that is important in cell adhesion. To further investigate the molecular basis of this notion, we used small-interfering RNA to inhibit E-cadherin function and found that loss of E-cadherin promoted Colorectal cancer cell growth, invasion and drug resistance through induction of β-catenin nuclear translocation and epithelial-to-mesenchymal transition. Further analysis of E-cadherin expression with clinicopathologic parameters showed that E-cadherin expression decreased in Colorectal cancer patients who developed liver metastasis (P = 0.043). These findings indicate that E-cadherin loss in tumors contributes to progression and metastatic dissemination. Thus, E-cadherin can act as a central modulator of the cell biological phenotypes and a potential prognostic marker in Colorectal cancer.

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References

    1. Oncogene. 2001 Aug 16;20(36):4942-50 - PubMed
    1. Nat Rev Cancer. 2003 Jun;3(6):453-8 - PubMed
    1. Ann Surg. 2008 Dec;248(6):968-78 - PubMed
    1. Cell Biol Int. 2002;26(5):463-76 - PubMed
    1. Oncology. 2006;71(1-2):102-10 - PubMed

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