Deciphering the loop of epithelial-mesenchymal transition, inflammatory cytokines and cancer immunoediting

Cytokine Growth Factor Rev. 2017 Aug:36:67-77. doi: 10.1016/j.cytogfr.2017.05.008. Epub 2017 May 31.

Abstract

Tumorigenesis and tumor progression relies on the dialectics between tumor cells, the extracellular matrix and its remodelling enzymes, neighbouring cells and soluble cues. The host immune response is crucial in eliminating or promoting tumor growth and the reciprocal coevolution of tumor and immune cells, during disease progression and in response to therapy, shapes tumor fate by activating innate and adaptive mechanisms. The phenotypic plasticity is a common feature of epithelial and immune cells and epithelial-mesenchymal transition (EMT) is a dynamic process, governed by microenvironmental stimuli, critical in tumor cell shaping, increased tumor cell heterogeneity and stemness. In this review we will outline how the dysregulation of microenvironmental signaling is crucial in determining tumor plasticity and EMT, arguing how therapy resistance hinges on these dynamics.

Keywords: CSC; EMT; Tumor immunoediting; Tumor microenvironment.

Publication types

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

MeSH terms

  • Animals
  • Cell Transformation, Neoplastic
  • Cytokines / physiology*
  • Disease Progression
  • Epithelial-Mesenchymal Transition*
  • Extracellular Matrix / physiology
  • Humans
  • Inflammation
  • Mice
  • Neoplasms / genetics
  • Neoplasms / immunology*
  • Neoplasms / pathology
  • Neoplasms / physiopathology*
  • Neoplastic Stem Cells / physiology
  • Signal Transduction
  • Tumor Microenvironment* / immunology

Substances

  • Cytokines