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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

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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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Acknowledgments

This work was supported by Grant of Ministry of Health and Henan Medical Science and Technique Foundation (2011056), Henan Science and Technique Foundation (200538) and Henan Society Public Welfare Project (2008).

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No potential conflicts of interest were disclosed.

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Correspondence to Hongping Xia or Minghua Hu.

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Xiaobing Chen, Yongsheng Wang and Hongping Xia have contributed equally to this work.

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Chen, X., Wang, Y., Xia, H. et al. Loss of E-cadherin promotes the growth, invasion and drug resistance of colorectal cancer cells and is associated with liver metastasis. Mol Biol Rep 39, 6707–6714 (2012). https://doi.org/10.1007/s11033-012-1494-2

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  • DOI: https://doi.org/10.1007/s11033-012-1494-2

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