EMT as the ultimate survival mechanism of cancer cells

Semin Cancer Biol. 2012 Jun;22(3):194-207. doi: 10.1016/j.semcancer.2012.02.013. Epub 2012 Mar 8.

Abstract

Epithelial cancers make up the vast majority of cancer types and, during the transition from benign adenoma to malignant carcinoma and metastasis, epithelial tumor cells acquire a de-differentiated, migratory and invasive behavior. This process of epithelial-mesenchymal transition (EMT) goes along with dramatic changes in cellular morphology, the loss and remodeling of cell-cell and cell-matrix adhesions, and the gain of migratory and invasive capabilities. EMT itself is a multistage process, involving a high degree of cellular plasticity and a large number of distinct genetic and epigenetic alterations, as fully differentiated epithelial cells convert into poorly differentiated, migratory and invasive mesenchymal cells. In the past years, a plethora of genes have been identified that are critical for EMT and metastasis formation. Notably, the EMT process not only induces increased cancer cell motility and invasiveness but also allows cancer cells to avoid apoptosis, anoikis, oncogene addiction, cellular, senescence and general immune defense. Notably, EMT seems to play a critical role in the generation and maintenance of cancer stem cells, highly consistent with the notion that metastatic cells carry the ability to initiate new tumors.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Cadherins / genetics
  • Cadherins / physiology
  • Cell Differentiation / physiology
  • Cell Transformation, Neoplastic / genetics*
  • Cell Transformation, Neoplastic / metabolism
  • Cell-Matrix Junctions / genetics
  • Cell-Matrix Junctions / pathology*
  • Disease Progression
  • Epithelial-Mesenchymal Transition / genetics*
  • Epithelial-Mesenchymal Transition / physiology
  • Gene Expression Regulation, Neoplastic
  • Humans
  • MicroRNAs / metabolism
  • Neoplasm Metastasis / genetics
  • Neoplasm Metastasis / pathology*
  • Neoplasm Metastasis / physiopathology
  • Neoplastic Stem Cells / metabolism
  • Neoplastic Stem Cells / pathology*
  • Signal Transduction / physiology
  • Transcription Factors / physiology

Substances

  • Cadherins
  • MicroRNAs
  • Transcription Factors