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Related Experiment Video

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An Enzyme- and Serum-free Neural Stem Cell Culture Model for EMT Investigation Suited for Drug Discovery

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Published on: August 23, 2016

Hijacking EMT: Better Fat Than Dead.

Stefan Hinz¹, Mark A LaBarge¹

¹Department of Population Sciences, Beckman Research Institute at City of Hope, Duarte, CA 91010, USA.

|January 16, 2019

Summary

This summary is machine-generated.

Cancer cells spread through the epithelial-to-mesenchymal transition (EMT) program. Researchers found that EMT plasticity can be used to turn cancer cells into fat cells, stopping metastasis.

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Area of Science:

Oncology
Cell Biology
Cancer Metastasis Research

Background:

Cancer metastasis, the spread of cancer cells to distant sites, is a major cause of cancer-related mortality.
The epithelial-to-mesenchymal transition (EMT) is a cellular program critical for initiating cancer cell dissemination and metastasis.
Understanding the plasticity of the EMT program is key to developing novel anti-metastatic strategies.

Purpose of the Study:

To investigate the potential of exploiting the epithelial-to-mesenchymal transition (EMT) plasticity for therapeutic benefit.
To determine if cancer cells undergoing EMT can be redirected into alternative cell fates.
To explore a novel strategy for preventing cancer metastasis by inhibiting cell dissemination.

Main Methods:

Utilizing a mouse model of cancer.
Inducing and analyzing the epithelial-to-mesenchymal transition (EMT) program in cancer cells.
Employing lineage tracing and cellular fate mapping techniques.
Assessing the metastatic potential of manipulated cancer cells.

Main Results:

Demonstrated that the plasticity inherent in the EMT program can be harnessed to influence cancer cell fate.
Showcased the successful differentiation of disseminating cancer cells into post-mitotic adipocytes (fat cells).
Confirmed that this adipocyte differentiation effectively prevents the formation of metastases.

Conclusions:

The epithelial-to-mesenchymal transition (EMT) program's plasticity offers a unique therapeutic target.
Redirecting cancer cells towards an adipocyte fate is a viable strategy to block metastasis.
This approach holds promise for developing new treatments to prevent cancer spread.