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Updated: Aug 15, 2026

Defining Gene Functions in Tumorigenesis by Ex vivo Ablation of Floxed Alleles in Malignant Peripheral Nerve Sheath Tumor Cells
Published on: August 25, 2021
RECKing MMP function: implications for cancer development
Jin-Sae Rhee1, Lisa M Coussens
1Medical Scientist Training Program and Cancer Research Institute, University of California, San Francisco, 2340 Sutter St, 94143, USA.
Abstract:
Cancer is a multistage process requiring progressive genetic and epigenetic changes in neoplastic and responding stromal cells. Many alterations that occur during the process of malignant progression are regulated by the matrix metalloproteinase (MMP) family of extracellular proteases and their endogenous inhibitors. Recent work has identified a new cell-surface inhibitor of MMPs - RECK. RECK regulates MMP-induced pericellular signaling cascades during embryogenesis and tumorigenesis. Homozygous loss of RECK results in embryonic lethality and attenuated tumor development in adults - thus providing further support for an efficacious role for protease inhibitors as anticancer therapeutics.
Insights
RECK, a novel cell-surface inhibitor, regulates matrix metalloproteinases (MMPs) involved in cancer progression. Loss of RECK impairs tumor development, supporting protease inhibitors as cancer therapeutics.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Cancer involves genetic and epigenetic changes in tumor and stromal cells.
- Matrix metalloproteinases (MMPs) regulate malignant progression.
- RECK is a newly identified cell-surface inhibitor of MMPs.
Purpose of the Study:
- To investigate the role of RECK in regulating MMPs.
- To understand RECK's function in embryogenesis and tumorigenesis.
- To evaluate protease inhibitors as anticancer therapeutics.
Main Methods:
- Analysis of RECK's function in cellular signaling.
- Studying the effects of RECK deficiency in embryonic development.
- Assessing tumor development in adult models with RECK loss.
Main Results:
- RECK regulates MMP-induced pericellular signaling.
- Homozygous loss of RECK leads to embryonic lethality.
- RECK deficiency attenuates tumor development in adult organisms.
Conclusions:
- RECK plays a crucial role in development and tumor suppression.
- Targeting MMPs via inhibitors like RECK shows therapeutic potential for cancer.
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