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Updated: Sep 27, 2025

An In Ovo Model for Testing Insulin-mimetic Compounds
Published on: April 23, 2018
Insulin-Degrading Enzyme, an Under-Estimated Potential Target to Treat Cancer?
Laetitia Lesire1, Florence Leroux1, Rebecca Deprez-Poulain1
1INSERM U1177 Drugs and Molecules for Living Systems, Institut Pasteur de Lille, European Genomic Institute for Diabetes, University of Lille, F-59000 Lille, France.
Abstract:
Insulin-degrading enzyme (IDE) is a multifunctional protease due to the variety of its substrates, its various cellular locations, its conservation between species and its many non-proteolytic functions. Numerous studies have successfully demonstrated its implication in two main therapeutic areas: metabolic and neuronal diseases. In recent years, several reports have underlined the overexpression of this enzyme in different cancers. Still, the exact role of IDE in the physiopathology of cancer remains to be elucidated. Known as the main enzyme responsible for the degradation of insulin, an essential growth factor for healthy cells and cancer cells, IDE has also been shown to behave like a chaperone and interact with the proteasome. The pharmacological modulation of IDE (siRNA, chemical compounds, etc.) has demonstrated interesting results in cancer models. All these results point towards IDE as a potential target in cancer. In this review, we will discuss evidence of links between IDE and cancer development or resistance, IDE's functions, catalytic or non-catalytic, in the context of cell proliferation, cancer development and the impact of the pharmacomodulation of IDE via cancer therapeutics.
Insights
Insulin-degrading enzyme (IDE) is implicated in metabolic and neuronal diseases. Emerging evidence suggests IDE
Area of Science:
- Biochemistry
- Molecular Biology
- Oncology
Background:
- Insulin-degrading enzyme (IDE) is a multifunctional protease with diverse substrates and cellular roles.
- IDE is known for its involvement in metabolic and neuronal diseases.
- Recent findings indicate IDE overexpression in various cancers, prompting investigation into its oncogenic role.
Purpose of the Study:
- To review the evidence linking IDE to cancer development and resistance.
- To elucidate the catalytic and non-catalytic functions of IDE in cancer cell proliferation.
- To discuss the impact of IDE pharmacomodulation as a potential cancer therapeutic strategy.
Main Methods:
- Literature review of studies on IDE and cancer.
- Analysis of IDE's known functions, including insulin degradation, chaperone activity, and proteasome interaction.
- Examination of preclinical data on IDE inhibition in cancer models.
Main Results:
- IDE plays a role in cancer development and resistance through various mechanisms.
- IDE's functions, both catalytic and non-catalytic, influence cancer cell proliferation.
- Pharmacological modulation of IDE has shown promising results in preclinical cancer studies.
Conclusions:
- IDE is emerging as a significant factor in cancer physiopathology.
- IDE's multifaceted roles suggest it is a potential therapeutic target in oncology.
- Targeting IDE offers a promising avenue for novel cancer treatment strategies.
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