The DOI matches its Crossref record; 3 of the 3 references it cites were found in a registry or an index.
NF-κB is essential for epithelial-mesenchymal transition and metastasis in a model of breast cancer progression
Open accessAbstract
The transcription factor NF-kappaB is activated in a range of human cancers and is thought to promote tumorigenesis, mainly due to its ability to protect transformed cells from apoptosis. To investigate the role of NF-kappaB in epithelial plasticity and metastasis, we utilized a well-characterized in vitro/in vivo model of mammary carcinogenesis that depends on the collaboration of the Ha-Ras oncoprotein and TGF-beta. We show here that the IKK-2/IkappaBalpha/NF-kappaB pathway is required for the induction and maintenance of epithelial-mesenchymal transition (EMT). Inhibition of NF-kappaB signaling prevented EMT in Ras-transformed epithelial cells, while activation of this pathway promoted the transition to a mesenchymal phenotype even in the absence of TGF-beta. Furthermore, inhibition of NF-kappaB activity in mesenchymal cells caused a reversal of EMT, suggesting that NF-kappaB is essential for both the induction and maintenance of EMT. In line with the importance of EMT for invasion, blocking of NF-kappaB activity abrogated the metastatic potential of mammary epithelial cells in a mouse model system. Collectively, these data provide evidence of an essential role for NF-kappaB during distinct steps of breast cancer progression and suggest that the cooperation of Ras- and TGF-beta-dependent signaling pathways in late-stage tumorigenesis depends critically on NF-kappaB activity.
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Cites
Activators and target genes of Rel/NF-κB transcription factors
Pahl, H. L. (1999) · Oncogene · doi:10.1038/sj.onc.1203239 · Cited by 3,727
IκB Kinase Promotes Tumorigenesis through Inhibition of Forkhead FOXO3a
Hu, M. C.-T., Lee, D.-F., Xia, W., Golfman, L. S., Ou-Yang, F., Yang, J.-Y., Zou, Y., Bao, S., Hanada, N., Saso, H., et al. (2004) · Cell · doi:10.1016/s0092-8674(04)00302-2 · Cited by 868
Helbig, G., Christopherson, K. W., Bhat-Nakshatri, P., Kumar, S., Kishimoto, H., Miller, K. D., Broxmeyer, H. E., & Nakshatri, H. (2003) · Journal of Biological Chemistry · doi:10.1074/jbc.m300609200 · Cited by 639
Cited by
Epithelial-Mesenchymal Transitions in Development and Disease
Thiery, J. P., Acloque, H., Huang, R. Y. J., & Nieto, M. A. (2009) · Cell · doi:10.1016/j.cell.2009.11.007 · Cited by 9,931
NF-κB, inflammation, immunity and cancer: coming of age
Taniguchi, K., & Karin, M. (2018) · Nature Reviews Immunology · doi:10.1038/nri.2017.142 · Cited by 2,679
Guidelines and definitions for research on epithelial-mesenchymal transition
Yang, J., Antin, P., Berx, G., Blanpain, C., Brabletz, T., Bronner, M., Campbell, K., Cano, A., Casanova, J., Christofori, G., et al. (2020) · Nature Reviews Molecular Cell Biology · doi:10.1038/s41580-020-0237-9 · Cited by 2,226
Immune checkpoint inhibitors: recent progress and potential biomarkers
Darvin, P., Toor, S. M., Sasidharan Nair, V., & Elkord, E. (2018) · Experimental & Molecular Medicine · doi:10.1038/s12276-018-0191-1 · Cited by 2,035
Labelle, M., Begum, S., & Hynes, R. O. (2011) · Cancer Cell · doi:10.1016/j.ccr.2011.09.009 · Cited by 1,833
Metadata
- Authors
- Huber, M. A., Azoitei, N., Baumann, B., Grünert, S., Sommer, A., Pehamberger, H., Kraut, N., Beug, H., & Wirth, T.
- Venue
- Journal of Clinical Investigation
- Published
- 2004-08-16
- Volume
- 114
- Issue
- 4
- Pages
- 569-581
- ISSN
- 0021-9738 (ISSN-L)
- OpenAlex
- W2141290206
- Cited by
- 1,033
- References
- 3
- FWCI
- 12.61
- Type
- journal article
- Language
- en
- Open access
- bronze
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- Huber, M. A., Azoitei, N., Baumann, B., Grünert, S., Sommer, A., Pehamberger, H., Kraut, N., Beug, H., & Wirth, T. (2004). NF-κB is essential for epithelial-mesenchymal transition and metastasis in a model of breast cancer progression. Journal of Clinical Investigation. https://doi.org/10.1172/jci200421358
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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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