Epithelial-mesenchymal transition and breast cancer: role, molecular mechanisms and clinical impact

Cancer Treat Rev. 2012 Oct;38(6):689-97. doi: 10.1016/j.ctrv.2011.11.001. Epub 2011 Nov 26.

Abstract

Epithelial-mesenchymal transition (EMT) is defined by the loss of epithelial characteristics and the acquisition of a mesenchymal phenotype. In this process, cells acquire molecular alterations that facilitate dysfunctional cell-cell adhesive interactions and junctions. These processes may promote cancer cell progression and invasion into the surrounding microenvironment. Such transformation has implications in progression of breast carcinoma to metastasis, and increasing evidences support most tumors contain a subpopulation of cells with stem-like and mesenchymal features that is resistant to chemotherapy. This review focuses on the physiological and pathological role of EMT process, its molecular related network, its putative role in the metastatic process and its implications in response/resistance to the current and/or new approaching drugs in the clinical management of breast cancer.

Publication types

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

MeSH terms

  • Antineoplastic Agents / pharmacology
  • Antineoplastic Agents / therapeutic use
  • Biomarkers / metabolism
  • Breast Neoplasms / metabolism*
  • Breast Neoplasms / pathology*
  • Breast Neoplasms / therapy
  • Cell Transformation, Neoplastic / drug effects
  • Cell Transformation, Neoplastic / metabolism
  • Drug Resistance, Neoplasm
  • Epithelial-Mesenchymal Transition* / drug effects
  • Female
  • Humans
  • Molecular Targeted Therapy
  • Neoplasm Metastasis
  • Neoplastic Cells, Circulating
  • Signal Transduction / drug effects

Substances

  • Antineoplastic Agents
  • Biomarkers