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Cited by 593

The DOI matches its Crossref record; 50 of the 50 references it cites were found in a registry or an index.

NF-κB–YY1–miR-29 Regulatory Circuitry in Skeletal Myogenesis and Rhabdomyosarcoma

Open access
Wang, Huating, Garzon, Ramiro, Sun, Hao, Ladner, Katherine J., Singh, Ravi, Dahlman, Jason, Cheng, Alfred, Hall, Brett M., Qualman, Stephen J., Chandler, Dawn S., Croce, Carlo M., Guttridge, Denis C.·2008·Cancer Cell
DOI 10.1016/j.ccr.2008.10.006
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Abstract

SUMMARY Studies support the importance of microRNAs in physiological and pathological processes. Here we describe the regulation and function of miR-29 in myogenesis and Rhabdomyosarcoma (RMS). Results demonstrate that in myoblasts miR-29 is repressed by NF-κB acting through YY1 and the Polycomb. During myogenesis, NF-κB and YY1 downregulation causes derepression of miR-29, which in turn accelerates differentiation by targeting its repressor YY1. However, in RMS cells and primary tumors that possess impaired differentiation, miR-29 is epigenetically silenced by an activated NF-κB-YY1 pathway. Reconstitution of miR-29 in RMS in mice inhibits tumor growth and stimulates differentiation, suggesting that miR-29 acts as a tumor suppressor through its pro-myogenic function. Together, results identify a NF-κB–YY1–miR-29 regulatory circuit whose disruption may contribute to RMS. SIGNIFICANCE MicroRNAs regulate skeletal myogenesis, but their impact in muscle diseases is not well understood. Here we describe miR-29 as an enhancer of myogenic differentiation and a suppressor of RMS. We find that miR-29 exists in a regulatory circuit involving NF-κB and YY1. In myoblasts NF-B acts through YY1 to epigenetically suppress miR-29, while during differentiation miR-29 is induced to facilitate myogenesis by a negative feedback on YY1. Significantly, RMS tumors lose miR-29 due to an elevation in NF-B and YY1, and readjustment of miR-29 levels in RMS stimulates differentiation. Thus, myogenesis is dependent on NF-κB–YY1–miR-29 circuitry whose dysfunction may contribute to RMS pathogenesis. Such findings offer potential avenues for the diagnosis and treatment of muscle relevant cancers.

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Metadata

Authors
Wang, H., Garzon, R., Sun, H., Ladner, K. J., Singh, R., Dahlman, J., Cheng, A., Hall, B. M., Qualman, S. J., Chandler, D. S., Croce, C. M., & Guttridge, D. C.
Venue
Cancer Cell
Publisher
Elsevier BV
Published
2008-11
Volume
14
Issue
5
Pages
369-381
ISSN
1535-6108 (ISSN-L)
DOI
10.1016/j.ccr.2008.10.006
OpenAlex
W2058484411
Cited by
593
References
50
FWCI
11.83
Type
journal article
Language
en
Open access
bronze

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CoChat. (2026). Citation check: NF-κB–YY1–miR-29 Regulatory Circuitry in Skeletal Myogenesis and Rhabdomyosarcoma. https://app.cochat.ai/papers/10.1016/j.ccr.2008.10.006
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Wang, H., Garzon, R., Sun, H., Ladner, K. J., Singh, R., Dahlman, J., Cheng, A., Hall, B. M., Qualman, S. J., Chandler, D. S., Croce, C. M., & Guttridge, D. C. (2008). NF-κB–YY1–miR-29 Regulatory Circuitry in Skeletal Myogenesis and Rhabdomyosarcoma. Cancer Cell. https://doi.org/10.1016/j.ccr.2008.10.006

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

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