ArticleLife science alliance2022
Proteins implicated in muscular dystrophy and cancer are functional constituents of the centrosome.
Article in Life science alliance, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 4 citations in OpenAlex.
- Calpains as Potential Regulators of Microtubule-Associated Cytokinesis: A Cross-Eukaryotic Unifying Hypothesis.Life (Basel, Switzerland) · 2026Article
- Frequent expression of aberrant chimeric Cdkn2a transcripts in mouse models of muscular dystrophy.Scientific reports · 2026Article
- Ubiquitination-targeted therapies improve BMD iPSC myogenic cell engraftment and dystrophin expressionMolecular therapy. Methods & clinical development · 2025Article
- Biallelic NSUN3 Variants Cause Diverse Phenotypic Spectrum Disease: From Isolated Optic Atrophy to Severe Early-Onset Mitochondrial Disorder.Investigative ophthalmology & visual science · 2025Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Aberrant expression of dystrophin, utrophin, dysferlin, or calpain-3 was originally identified in muscular dystrophies (MDs). Increasing evidence now indicates that these proteins might act as tumor suppressors in myogenic and non-myogenic cancers. As DNA damage and somatic aneuploidy, hallmarks of cancer, are early pathological signs in MDs, we hypothesized that a common pathway might involve the centrosome. Here, we show that dystrophin, utrophin, dysferlin, and calpain-3 are functional constituents of the centrosome. In myoblasts, lack of any of these proteins caused excess centrosomes, centrosome misorientation, nuclear abnormalities, and impaired microtubule nucleation. In dystrophin double-mutants, these defects were significantly aggravated. Moreover, we demonstrate that also in non-myogenic cells, all four MD-related proteins localize to the centrosome, including the muscle-specific full-length dystrophin isoform. Therefore, MD-related proteins might share a convergent function at the centrosome in addition to their diverse, well-established muscle-specific functions. Thus, our findings support the notion that cancer-like centrosome-related defects underlie MDs and establish a novel concept linking MDs to cancer.
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Registered trials
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