The DOI matches its Crossref record; 40 of the 40 references it cites were found in a registry or an index.
Breast cancer bone metastasis mediated by the Smad tumor suppressor pathway
Open accessAbstract
TGF-β can signal by means of Smad transcription factors, which are quintessential tumor suppressors that inhibit cell proliferation, and by means of Smad-independent mechanisms, which have been implicated in tumor progression. Although Smad mutations disable this tumor-suppressive pathway in certain cancers, breast cancer cells frequently evade the cytostatic action of TGF-β while retaining Smad function. Through immunohistochemical analysis of human breast cancer bone metastases and functional imaging of the Smad pathway in a mouse xenograft model, we provide evidence for active Smad signaling in human and mouse bone-metastatic lesions. Genetic depletion experiments further demonstrate that Smad4 contributes to the formation of osteolytic bone metastases and is essential for the induction of IL-11 , a gene implicated in bone metastasis in this mouse model system. Activator protein-1 is a key participant in Smad-dependent transcriptional activation of IL - 11 and its overexpression in bone-metastatic cells. Our findings provide functional evidence for a switch of the Smad pathway, from tumor-suppressor to prometastatic, in the development of breast cancer bone metastasis.
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Cites
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Cited by
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Metadata
- Authors
- Kang, Y., He, W., Tulley, S., Gupta, G. P., Serganova, I., Chen, C.-R., Manova-Todorova, K., Blasberg, R., Gerald, W. L., & Massagué, J.
- Venue
- Proceedings of the National Academy of Sciences
- Published
- 2005-09-19
- Volume
- 102
- Issue
- 39
- Pages
- 13909-13914
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- OpenAlex
- W2116403488
- Cited by
- 532
- References
- 40
- FWCI
- 13.37
- Type
- journal article
- Language
- en
- Open access
- green
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- Kang, Y., He, W., Tulley, S., Gupta, G. P., Serganova, I., Chen, C.-R., Manova-Todorova, K., Blasberg, R., Gerald, W. L., & Massagué, J. (2005). Breast cancer bone metastasis mediated by the Smad tumor suppressor pathway. Proceedings of the National Academy of Sciences. https://doi.org/10.1073/pnas.0506517102
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