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Related Concept Videos

The Tumor Microenvironment02:17

The Tumor Microenvironment

Every normal cell or tissue is embedded in a complex local environment called stroma, consisting of different cell types, a basal membrane, and blood vessels. As normal cells mutate and develop into cancer cells, their local environment also changes to allow cancer progression. The tumor microenvironment (TME) consists of a complex cellular matrix of stromal cells and the developing tumor. The cross-talk between cancer cells and surrounding stromal cells is critical to disrupt normal tissue...
The Tumor Microenvironment02:17

The Tumor Microenvironment

Every normal cell or tissue is embedded in a complex local environment called stroma, consisting of different cell types, a basal membrane, and blood vessels. As normal cells mutate and develop into cancer cells, their local environment also changes to allow cancer progression. The tumor microenvironment (TME) consists of a complex cellular matrix of stromal cells and the developing tumor. The cross-talk between cancer cells and surrounding stromal cells is critical to disrupt normal tissue...
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Epithelial-to-Mesenchymal Transition
The epithelial-to-mesenchymal transition or EMT is a developmental process commonly observed in wound healing, embryogenesis, and cancer metastasis. EMT is induced by transforming growth factor-beta (TGF-β) or receptor tyrosine kinase (RTK) ligands, which further...
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The cadherins are a superfamily of cell adhesion molecules comprising over 180 variants, with specific tissues expressing a particular combination of cadherin types. Cadherins generally exhibit homophilic binding; i.e., cadherins on one cell bind to cadherins of the same or closely related type on another cell. Thus, cells of the same type have a specific affinity to bind to each other and sort themselves into clusters to form tissues.
Cell Sorting During Development
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Mitogens and their receptors play a crucial role in controlling the progression of the cell cycle. However, the loss of mitogenic control over cell division leads to tumor formation. Therefore, mitogens and mitogen receptors play an important role in cancer research. For instance, the epidermal growth factor (EGF) - a type of mitogen and its transmembrane receptor (EGFR), decides the fate of the cell's proliferation. When EGF binds to EGFR, a member of the ErbB family of tyrosine kinase...
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Induction of Mesenchymal-Epithelial Transitions in Sarcoma Cells
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Epithelial-Mesenchymal Transition in tumor microenvironment.

Yingying Jing1, Zhipeng Han, Shanshan Zhang

  • 1Tumor Immunology and Gene Therapy Center, Eastern Hepatobiliary Surgery Hospital, the Second Military Medicial University, Shanghai, China. lixinwei@smmu.edu.cn.

Cell & Bioscience
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PubMed
Summary

The tumor microenvironment, including inflammation and hypoxia, drives epithelial to mesenchymal transition (EMT). This process promotes cancer metastasis through various signaling pathways.

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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
  • Molecular Biology

Background:

  • Epithelial to mesenchymal transition (EMT) is critical for embryonic development and tumor invasion.
  • EMT involves loss of cell adhesion, polarity changes, and increased motility, facilitating cancer metastasis.
  • The tumor microenvironment (TME) significantly influences EMT and cancer progression.

Purpose of the Study:

  • To review the role of the tumor microenvironment in inducing EMT.
  • To discuss signaling pathways implicated in TME-driven EMT.
  • To explore the interplay between the TME and EMT signaling.

Main Methods:

  • Literature review of existing research on EMT, TME, and cancer metastasis.
  • Analysis of signaling pathways (e.g., TGF-β, NF-κB, Wnt, Notch) involved in EMT.
  • Synthesis of current knowledge on TME components as EMT inducers.

Main Results:

  • The TME contains factors like inflammatory cells, hypoxia, cancer stem cells (CSCs), and mesenchymal stem cells (MSCs) that promote EMT.
  • Specific signaling pathways are activated within the TME to drive EMT.
  • Complex interactions exist between TME components and EMT signaling pathways.

Conclusions:

  • The TME is a key regulator of EMT, promoting tumor invasion and metastasis.
  • Targeting TME-induced EMT and its signaling pathways offers potential therapeutic strategies.
  • Further research is needed to fully elucidate the TME-EMT axis for cancer treatment.