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Epithelial to Mesenchymal Transition: A Mechanism that Fuels Cancer Radio/Chemoresistance

József Dudas1, Andrea Ladanyi2, Julia Ingruber1

  • 1Department of Otorhinolaryngology and Head and Neck Surgery, Medical University of Innsbruck, 6020 Innsbruck, Austria.

Cells
|February 16, 2020
PubMed

Insights

Epithelial to mesenchymal transition (EMT) drives tumor progression and therapy resistance. Understanding EMT

Area of Science:

  • Oncology and Molecular Biology: Focuses on cellular processes driving cancer progression.

Background:

  • Epithelial to mesenchymal transition (EMT) is a cellular process crucial for tumor progression, invasion, and therapy resistance.
  • EMT is orchestrated by transcription factors (e.g., SNAI gene family) and signaling pathways (e.g., TGF-beta1, IL-6, Akt, Erk1/2).
  • Non-coding RNAs, including microRNAs and long non-coding RNAs, also play a role in initiating EMT.

Purpose of the Study:

  • To explore the complex interplay between the tumor microenvironment and EMT.
  • To understand how microenvironmental factors influence EMT and subsequent tumor cell behavior.
  • To highlight the role of EMT in shaping the tumor microenvironment.

Main Methods:

  • Review of current literature on EMT regulation and microenvironment interactions.
  • Analysis of signaling pathways and molecular mechanisms involved in EMT.
  • Investigation of cellular components within the tumor microenvironment that influence EMT.

Main Results:

  • Tumor microenvironment components (fibroblasts, immune cells, endothelial cells) actively induce EMT in cancer cells.
  • EMT promotes a shift in the tumor microenvironment, fostering immune suppression (regulatory T cells, exhausted CD8+ T cells, M2 macrophages).
  • EMT tumor cells actively remodel their microenvironment to support tumor growth.

Conclusions:

  • EMT is a dynamic process influenced by and influencing the tumor microenvironment.
  • Targeting EMT and its microenvironmental interactions presents promising therapeutic strategies.
  • Understanding these mechanisms is critical for developing effective cancer treatments.
Keywords:
Krüppel-like factors (KLFs)MRX34NRF2PD-L1neurotrophinsilibinin

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