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Updated: Aug 17, 2026

Identification of MyoD Interactome Using Tandem Affinity Purification Coupled to Mass Spectrometry
Published on: May 17, 2016
The membrane-anchored MMP-regulator RECK is a target of myogenic regulatory factors
Michiko Echizenya1, Shunya Kondo, Rei Takahashi
1Department of Molecular Oncology, Kyoto University Graduate School of Medicine, Yoshida-Konoe-cho, Sakyo-ku, Japan.
Abstract:
The membrane-anchored MMP-regulator RECK is down regulated in many solid tumors; the extent of RECK down regulation correlates with poor prognosis. Forced expression of RECK in tumor cells results in suppression of angiogenesis, invasion, and metastasis. Studies on the roles and the mechanisms of regulation of the RECK gene during normal development may therefore yield important insights into how the malignant behaviors of tumor cells arise and how they can be controlled. Our previous studies indicate that mice lacking RECK die around E10.5 with reduced tissue integrity. In the present study, we have found that in later stage wild-type embryos, RECK is abundantly expressed in skeletal muscles, especially in the areas where the myoblast differentiation factor MRF4 is expressed. Consistent with this finding, the RECK-promoter is activated by MRF4 in cultured cells. In contrast, a myoblast determination factor MyoD suppresses the RECK-promoter. Myoblastic cells lacking RECK expression give rise to myotubes at higher efficiency than the cells expressing RECK, indicating that RECK suppresses myotube formation. These findings suggest that MyoD down regulates RECK to facilitate myotube formation, whereas MRF4 up regulates RECK to promote other aspects of myogenesis that require extracellular matrix integrity.
Insights
RECK protein suppresses muscle cell (myotube) formation. MyoD reduces RECK to aid myotube development, while MRF4 increases RECK for other muscle-building processes, highlighting RECK
Area of Science:
- Molecular and Developmental Biology
- Cancer Research
- Muscle Development
Background:
- The RECK protein, a regulator of matrix metalloproteinases, is downregulated in many solid tumors, correlating with poor prognosis.
- Forced RECK expression in tumor cells inhibits angiogenesis, invasion, and metastasis.
- Understanding RECK's role in normal development offers insights into tumor cell malignancy and control.
Purpose of the Study:
- To investigate the role and regulation of the RECK gene during normal embryonic development, specifically in skeletal muscle.
- To elucidate the relationship between RECK expression and key muscle development factors like MyoD and MRF4.
Main Methods:
- Analysis of RECK expression patterns in later-stage wild-type mouse embryos.
- Investigated RECK promoter activity in cultured cells in response to MyoD and MRF4.
- Assessed myotube formation efficiency in myoblastic cells with varying RECK expression levels.
Main Results:
- RECK is abundantly expressed in skeletal muscles of wild-type embryos, particularly where MRF4 is present.
- MRF4 activates the RECK promoter, whereas MyoD suppresses it.
- Absence of RECK enhances myotube formation efficiency, indicating RECK suppresses this process.
Conclusions:
- MyoD downregulates RECK to promote myotube formation.
- MRF4 upregulates RECK to support other aspects of myogenesis requiring extracellular matrix integrity.
- RECK plays a dual role in myogenesis, balancing myotube formation with extracellular matrix maintenance.
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