ArticleOncogene2004
Myostatin inhibits rhabdomyosarcoma cell proliferation through an Rb-independent pathway.
Article in Oncogene, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
15 citing papers in PubMed, 55 citations in OpenAlex.
- CVB3 VP1 interacts with MAT1 to inhibit cell proliferation by interfering with Cdk-activating kinase complex activity in CVB3-induced acute pancreatitis.PLoS pathogens · 2021Article
- The Possible Role of Complete Loss of Myostatin in Limiting Excessive Proliferation of Muscle Cells (C2C12) via Activation of MicroRNAs.International journal of molecular sciences · 2019Article
- Article
- Prostaglandin E2 promotes proliferation of skeletal muscle myoblasts via EP4 receptor activation.Cell cycle (Georgetown, Tex.) · 2015Article
- Role of activin-A and myostatin and their signaling pathway in human myometrial and leiomyoma cell function.The Journal of clinical endocrinology and metabolism · 2014Article
- Myostatin inhibitors as therapies for muscle wasting associated with cancer and other disorders.Current opinion in supportive and palliative care · 2013Review
- Mechanisms of impaired differentiation in rhabdomyosarcoma.The FEBS journal · 2013Review
- Delta-like 1 homolog (dlk1): a marker for rhabdomyosarcomas implicated in skeletal muscle regeneration.PloS one · 2013Article
- Oral rhabdomyosarcoma: A review.Journal of clinical and experimental dentistry · 2012Review
- Myostatin is a novel tumoral factor that induces cancer cachexia.The Biochemical journal · 2012Article
- Rhabdomyosarcomas: an overview on the experimental animal models.Journal of cellular and molecular medicine · 2012Review
- Caveolins in rhabdomyosarcoma.Journal of cellular and molecular medicine · 2011Review
- Smad3 signaling is required for satellite cell function and myogenic differentiation of myoblasts.Cell research · 2011Article
- Checking before changing: cell cycle checkpoints inhibit muscle differentiation.Cell cycle (Georgetown, Tex.) · 2011Article
- Clinical, agricultural, and evolutionary biology of myostatin: a comparative review.Endocrine reviews · 2008Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Rhabdomyosarcoma (RMS) tumors are the most common soft-tissue sarcomas in childhood. In this investigation, we show that myostatin, a skeletal muscle-specific inhibitor of growth and differentiation is expressed and translated in the cultured RMS cell line, RD. The addition of exogenous recombinant myostatin inhibits the proliferation of RD cells cultured in growth media, consistent with the role of myostatin in normal myoblast proliferation inhibition. However, unlike normal myoblasts, upregulation of p21 was not observed. Rather, myostatin signalling resulted in the specific downregulation of both Cdk2 and its cognate partner, cyclin-E. The analysis of Rb reveals that there was no change in its phosphorylation status with myostatin treatment, consistent with D-type-cyclin-Cdk4/6 complexes being active in the absence of p21. Moreover, the activity of Rb appeared to be unchanged between treated and nontreated RD cells, as determined by the ability of Rb to bind E2F1. The examination of NPAT, a substrate of cyclin-E-Cdk2 involved in the transcriptional activation of replication-dependent histone gene expression, revealed that it undergoes a loss of phosphorylation with myostatin treatment. Supporting this, a downregulation in H4-histone gene expression was observed. These results suggest that myostatin could potentially be used as an inhibitor of RMS proliferation and define a previously uncharacterized, Rb-independent mechanism for the inhibition of muscle precursor cell proliferation by myostatin.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.