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CAM-Delam Assay to Score Metastatic Properties by Quantifying Delamination and Invasion Capacity of Cancer Cells
Published on: June 2, 2022
New potential therapeutic targets to combat epithelial tumor invasion
1Departamento de Bioquímica, Facultad de Medicina, Instituto de Investigaciones Biomédicas Alberto Sols, CSIC-UAM. Madrid. Spain. hpeinado@iib.uam.es
Abstract:
Metastasis is the deadly face of epithelial tumors. The studies performed in the last decade have shed considerable light on the processes involved in the metastatic cascade. In particular, much effort has focused on defining the molecular changes that govern the conversion from an epithelial to a mesenchymal cell, a process known as epithelial-mesenchymal transition (EMT). The process of EMT is considered a fundamental event in the metastatic cascade (i.e. during invasion and/or intravasation) and several molecules involved in EMT have been described, including epithelial markers, transcription factors, as well as extracellular proteins and growth factors. In this green series article, we will focus our attention on the new molecules described in the recent years that appear to influence EMT and that are therefore relevant to epithelial carcinogenesis. Furthermore, we will try to explain how these molecules collaborate with the tumor microenvironment to trigger metastasis. Recent advances in our understanding of this process is generating a wide range of molecules that could be potentially considered as new therapeutic targets for drug design to block metastatic spreading.
Insights
Metastasis, the spread of epithelial tumors, is driven by epithelial-mesenchymal transition (EMT). Recent research identifies new molecules influencing EMT and tumor microenvironment interactions, offering potential therapeutic targets for cancer drug design.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Research
Background:
- Metastasis is a critical hallmark of epithelial tumors, significantly impacting patient outcomes.
- The epithelial-mesenchymal transition (EMT) is a key cellular process in the metastatic cascade, involving significant molecular changes.
Purpose of the Study:
- To review recent discoveries of novel molecules involved in EMT.
- To elucidate the role of these molecules and their collaboration with the tumor microenvironment in driving metastasis.
- To identify potential new therapeutic targets for blocking metastatic spread.
Main Methods:
- Literature review focusing on recent scientific publications (last decade).
- Analysis of molecular mechanisms underlying EMT and its regulation.
- Exploration of interactions between cancer cells and the tumor microenvironment.
Main Results:
- Identification of newly described molecules that influence EMT.
- Understanding of how these molecules interact with the tumor microenvironment to promote metastasis.
- Highlighting the relevance of these molecules in epithelial carcinogenesis.
Conclusions:
- Recent advances have expanded the understanding of EMT and its regulators.
- New molecular players in EMT and metastasis offer promising avenues for therapeutic intervention.
- Targeting these molecules could lead to novel strategies for inhibiting cancer metastasis.
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