The DOI matches its Crossref record; 6 of the 6 references it cites were found in a registry or an index.
Mitochondrial Localized Stat3 Promotes Breast Cancer Growth via Phosphorylation of Serine 727
Open accessAbstract
Signal transducer and activator of transcription 3 (Stat3) is a key mediator in the development of many cancers. For 20 years, it has been assumed that Stat3 mediates its biological activities as a nuclear localized transcription factor activated by many cytokines. However, recent studies from this laboratory and others indicate that Stat3 has an independent function in the mitochondria (mitoStat3) where it controls the activity of the electron transport chain (ETC) and mediates Ras-induced transformation of mouse embryo fibroblasts. The actions of mitoStat3 in controlling respiration and Ras transformation are mediated by the phosphorylation state of serine 727. To address the role of mitoStat3 in the pathogenesis of cells that are transformed, we used 4T1 breast cancer cells, which form tumors that metastasize in immunocompetent mice. Substitution of Ser-727 for an alanine or aspartate in Stat3 that has a mitochondrial localization sequence, MLS-Stat3, has profound effects on tumor growth, complex I activity of the ETC, and accumulation of reactive oxygen species (ROS). Cells expressing MLS-Stat3(S727A) display slower tumor growth, decreased complex I activity of the ETC, and increased ROS accumulation under hypoxia compared with cells expressing MLS-Stat3. In contrast, cells expressing MLS-Stat3(S727D) show enhanced tumor growth and complex I activity and decreased production of ROS. These results highlight the importance of serine 727 of mitoStat3 in breast cancer and suggest a novel role for mitoStat3 in regulation of ROS concentrations through its action on the ETC. Background: A pool of the nuclear transcription factor Stat3 in the mitochondria (mitoStat3) controls respiration and Ras transformation. Results: Serine phosphorylation of mitoStat3 controls accumulation of reactive oxygen species and growth of breast cancer in mice. Conclusion: These results provide the first evidence for a mechanism by which mitoStat3 contributes to tumorigenesis. Significance: The data suggest new therapeutic approaches to treatment of breast cancer.
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Cites
Function of Mitochondrial Stat3 in Cellular Respiration
Wegrzyn, J., Potla, R., Chwae, Y.-J., Sepuri, N. B. V., Zhang, Q., Koeck, T., Derecka, M., Szczepanek, K., Szelag, M., Gornicka, A., et al. (2009) · Science · doi:10.1126/science.1164551 · Cited by 1,014
Self-citationBulua, A. C., Simon, A., Maddipati, R., Pelletier, M., Park, H., Kim, K.-Y., Sack, M. N., Kastner, D. L., & Siegel, R. M. (2011) · Journal of Experimental Medicine · doi:10.1084/jem.20102049 · Cited by 860
Mitochondrial respiratory complex I: Structure, function and implication in human diseases
Sharma, L., Lu, J., & Bai, Y. (2009) · Current Medicinal Chemistry · doi:10.2174/092986709787846578 · Cited by 438
STAT3 nuclear import is independent of tyrosine phosphorylation and mediated by importin-α3
Liu, L., McBride, K. M., & Reich, N. C. (2005) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0501643102 · Cited by 348
Roles of unphosphorylated STATs in signaling
Yang, J., & Stark, G. R. (2008) · Cell Research · doi:10.1038/cr.2008.41 · Cited by 347
Yakovlev, V. A., Bayden, A. S., Graves, P. R., Kellogg, G. E., & Mikkelsen, R. B. (2010) · Biochemistry · doi:10.1021/bi100564w · Cited by 56
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Cited by
Revisiting STAT3 signalling in cancer: new and unexpected biological functions
Yu, H., Lee, H., Herrmann, A., Buettner, R., & Jove, R. (2014) · Nature Reviews Cancer · doi:10.1038/nrc3818 · Cited by 2,137
Mitochondrial Stat3, the need for design thinking
Yang, R., & Rincon, M. (2016) · International Journal of Biological Sciences · doi:10.7150/ijbs.15153 · Cited by 147
Peiris-Pagès, M., Sotgia, F., & Lisanti, M. P. (2015) · Oncotarget · doi:10.18632/oncotarget.3828 · Cited by 115
Genini, D., Brambilla, L., Laurini, E., Merulla, J., Civenni, G., Pandit, S., D'Antuono, R., Perez, L., Levy, D. E., Pricl, S., et al. (2017) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1615730114 · Cited by 106
Yang, R., Lirussi, D., Thornton, T. M., Jelley-Gibbs, D. M., Diehl, S. A., Case, L. K., Madesh, M., Taatjes, D. J., Teuscher, C., Haynes, L., et al. (2015) · eLife · doi:10.7554/elife.06376 · Cited by 91
Metadata
- Authors
- Zhang, Q., Raje, V., Yakovlev, V. A., Yacoub, A., Szczepanek, K., Meier, J., Derecka, M., Chen, Q., Hu, Y., Sisler, J., Hamed, H., Lesnefsky, E. J., Valerie, K., Dent, P., & Larner, A. C.
- Venue
- Journal of Biological Chemistry
- Publisher
- Elsevier BV
- Published
- 2013-10
- Volume
- 288
- Issue
- 43
- Pages
- 31280-31288
- ISSN
- 0021-9258 (ISSN-L)
- OpenAlex
- W2069050894
- Cited by
- 188
- References
- 6
- FWCI
- 7.90
- Type
- journal article
- Language
- en
- Open access
- hybrid
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- Zhang, Q., Raje, V., Yakovlev, V. A., Yacoub, A., Szczepanek, K., Meier, J., Derecka, M., Chen, Q., Hu, Y., Sisler, J., Hamed, H., Lesnefsky, E. J., Valerie, K., Dent, P., & Larner, A. C. (2013). Mitochondrial Localized Stat3 Promotes Breast Cancer Growth via Phosphorylation of Serine 727. Journal of Biological Chemistry. https://doi.org/10.1074/jbc.m113.505057
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