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    N-cadherin promotes epithelial-mesenchymal transition and cancer stem cell-like traits via ErbB signaling in prostate cancer cells.
    • Authors:
    • Min Wang
      Tongji Medical College
      Dong Ren
      Capital Normal University
      Wei Guo
      Peking University People's Hospital
      Shuai Huang
      Southwest Jiaotong University
      Zeyu Wang
      School of Life Science and Technology
      Daqing | China
      Qiji Li
      Guiyang College of Traditional Chinese Medicine
      Hong Du
      Indiana University School of Medicine
      United States
      Libing Song
      Sun Yat-sen University
      Xinsheng Peng
      Zhejiang University
    Int J Oncol 2016 Feb 26;48(2):595-606. Epub 2015 Nov 26.
    Department of Orthopaedic Surgery, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong 510080, P.R. China.
    N-cadherin has been reported to be upregulated and associated with metastasis and poor prognosis in prostate cancer patients, however the underlying mechanism still remains puzzling. In the present study, we found that upregulation of N-cadherin enhanced, while downregulation of N-cadherin impaired the invasion, migration, and epithelial to mesenchymal transition (EMT) of prostate cancer (PCa) cells. Overexpression of N-cadherin increased the efficiency of colony and tumor spheroid formation and the stemness factor expression (including c-Myc, Klf4, Sox2 and Oct4), and vice versa. Furthermore, microarray analysis and western blot analysis mechanistically proved that N-cadherin activated ErbB signaling pathway by upregulating the expression of Grb2, pShc and pERK1/2. Importantly, the regulation of N-cadherin on EMT and stemness was counteracted by lapatinib, a specific ErbB signaling pathway inhibitor. Collectively, these findings demonstrate that N-cadherin regulates EMT and stemness of PCa cells via activating ErbB signaling pathway, which indicates the pivotal role of N-cadherin/ErbB axis in the metastasis of prostate cancer.

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