Tumor-Derived Exosomes Mediate the Instability of Cadherins and Promote Tumor Progression

Int J Mol Sci. 2019 Jul 26;20(15):3652. doi: 10.3390/ijms20153652.


Cadherins, including E-cadherin, N-cadherin, VE-cadherin, etc., are important adhesion molecules mediating intercellular junctions. The abnormal expression of cadherins is often associated with tumor development and progression. Epithelial-mesenchymal transition (EMT) is the most important step in the metastasis cascade and is accompanied by altered expression of cadherins. Recent studies reveal that as a cargo for intercellular communication, exosomes-one type of extracellular vesicles that can be secreted by tumor cells-are involved in a variety of physiological and pathological processes, especially in tumor metastasis. Tumor-derived exosomes play a crucial role in mediating the cadherin instability in recipient cells by transferring bioactive molecules (oncogenic microRNAs (miRNAs) and long non-coding RNAs (lncRNAs), EMT-related proteins, and others), modulating their local and distant microenvironment, and facilitating cancer metastasis. In turn, aberrant expression of cadherins in carcinoma cells can also affect the biogenesis and release of exosomes. Therefore, we summarize the current research on the crosstalk between tumor-derived exosomes and aberrant cadherin signals to reveal the unique role of exosomes in cancer progression.

Keywords: cadherins; epithelial–mesenchymal transition; exosomes; long non-coding RNAs; microRNAs; tumor development.

Publication types

  • Review

MeSH terms

  • Animals
  • Biological Transport
  • Cadherins / metabolism*
  • Disease Progression
  • Epithelial-Mesenchymal Transition
  • Exosomes / metabolism*
  • Extracellular Vesicles / metabolism
  • Humans
  • MicroRNAs / genetics
  • MicroRNAs / metabolism
  • Neoplasms / etiology
  • Neoplasms / metabolism*
  • Neoplasms / pathology*
  • Protein Stability
  • RNA, Long Noncoding / genetics
  • RNA, Long Noncoding / metabolism


  • Cadherins
  • MicroRNAs
  • RNA, Long Noncoding