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Related Concept Videos

Somatic to iPS Cell Reprogramming01:29

Somatic to iPS Cell Reprogramming

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Induction of Mesenchymal-Epithelial Transitions in Sarcoma Cells
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The epithelial-mesenchymal transition under control: global programs to regulate epithelial plasticity.

M Angela Nieto1, Amparo Cano

  • 1Instituto de Neurociencias, CSIC-UMH. Av. Santiago Ramón y Cajal s/n, 03550 San Juan de Alicante, Spain. anieto@umh.es

Seminars in Cancer Biology
|May 23, 2012
PubMed
Summary

The epithelial to mesenchymal transition (EMT) is a dynamic process crucial for cancer metastasis. Understanding EMT as a reversible cellular plasticity is key to unraveling cancer progression and developing new therapies.

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Studying TGF-β Signaling and TGF-β-induced Epithelial-to-mesenchymal Transition in Breast Cancer and Normal Cells
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Studying TGF-β Signaling and TGF-β-induced Epithelial-to-mesenchymal Transition in Breast Cancer and Normal Cells

Published on: October 27, 2020

Area of Science:

  • Oncology
  • Cell Biology
  • Cancer Research

Background:

  • The epithelial to mesenchymal transition (EMT) is a significant area of cancer research, but its precise role in tumor biology and metastasis remains debated.
  • Viewing EMT as a reversible and often incomplete process, reflecting epithelial plasticity, offers a new perspective.

Purpose of the Study:

  • To clarify the controversial role of EMT in cancer metastasis.
  • To highlight the significance of transient cellular states in the metastatic cascade.
  • To explore the impact of EMT on various cellular responses relevant to cancer progression.

Main Methods:

  • Review and synthesis of current research on EMT in cancer.
  • Analysis of the concept of epithelial plasticity in the context of metastasis.
  • Examination of cellular programs influencing EMT and their downstream effects.

Main Results:

  • EMT is better understood as a reversible process, a form of epithelial plasticity, rather than a terminal differentiation.
  • Transient cellular states facilitate each step of metastasis, from detachment to colonization.
  • Cellular programs regulating EMT also influence proliferation, stemness, drug resistance, and immune responses.

Conclusions:

  • Reinterpreting EMT as a dynamic, plastic process is crucial for understanding cancer progression and metastasis.
  • The plasticity of EMT impacts multiple hallmarks of cancer, including resistance to therapy and immune evasion.
  • Further research into EMT dynamics can inform the development of novel anti-cancer strategies.