The DOI matches its Crossref record; 37 of the 37 references it cites were found in a registry or an index.
Oestrogen signalling inhibits invasive phenotype by repressing RelB and its target BCL2
Open accessAbstract
Aberrant constitutive expression of c-Rel, p65 and p50 NF-kappaB subunits has been reported in over 90% of breast cancers. Recently, we characterized a de novo RelB NF-kappaB subunit synthesis pathway, induced by the cytomegalovirus (CMV) IE1 protein, in which binding of p50-p65 NF-kappaB and c-Jun-Fra-2 AP-1 complexes to the RELB promoter work in synergy to potently activate transcription. Although RelB complexes were observed in mouse mammary tumours induced by either ectopic c-Rel expression or carcinogen exposure, little is known about RelB in human breast disease. Here, we demonstrate constitutive de novo RelB synthesis is selectively active in invasive oestrogen receptor alpha (ERalpha)-negative breast cancer cells. ERalpha signalling reduced levels of functional NF-kappaB and Fra-2 AP-1 and inhibited de novo RelB synthesis, leading to an inverse correlation between RELB and ERalpha gene expression in human breast cancer tissues and cell lines. Induction of Bcl-2 by RelB promoted the more invasive phenotype of ERalpha-negative cancer cells. Thus, inhibition of de novo RelB synthesis represents a new mechanism whereby ERalpha controls epithelial to mesenchymal transition (EMT).
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“These findings are in line with reported roles for the noncanonical NF-κB pathway in EMT, cellular invasion, and metastasis33–35.”
From Chromosomal instability drives metastasis through a cytosolic DNA response (2018) · cites this paper as [33]
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Cites
A Gene-Expression Signature as a Predictor of Survival in Breast Cancer
van de Vijver, M. J., He, Y. D., Veer, L. V. ‘., Dai, H. A., Hart, A. A. M., Voskuil, D. W., Schreiber, G. J., Peterse, J. L., Roberts, C., Marton, M. J., et al. (2002) · New England Journal of Medicine · doi:10.1056/nejmoa021967 · Cited by 6,474
Gene-expression profiles to predict distant metastasis of lymph-node-negative primary breast cancer
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Metastasis: a question of life or death
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bcl-2 inhibits multiple forms of apoptosis but not negative selection in thymocytes
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Constitutive Activation of NF-κB during Progression of Breast Cancer to Hormone-Independent Growth
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Expression of relB is required for the development of thymic medulla and dendritic cells
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Aberrant nuclear factor-kappaB/Rel expression and the pathogenesis of breast cancer.
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Self-citationTranscriptional regulation of bcl-2 by nuclear factor κB and its significance in prostate cancer
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Contribution à l’étude du rôle et de la régulation de Fra-1 dans le cancer
Milord, S. (2011) · theses.fr (ABES) · doi:10.70675/e0a1cbe3z67d5z4d8fzb19cz794e17b78d79
Régulation de l'invasion cellulaire induite par les tyrosine kinases dans le cancer du sein
Chevalier, C. (2014) · theses.fr (ABES) · doi:10.70675/692c8de1za82az4e5ez953bz5e90670eb75d
Involvements of Bcl-2 family of proteins during early zebrafish development
Popgeorgiev, N. (2011) · theses.fr (ABES) · doi:10.70675/d1fa4100z5c50z4a30z9f26z0ee43285ce5f
Modeling Hormone Receptor Positive Breast Cancer in Immunocompetent Mice
Pérez-Lanzón, M. (2021) · theses.fr (ABES) · doi:10.70675/8d0cd788z71c4z4627z898ezbb2b6500fa17
Prudent, J. (2011) · theses.fr (ABES) · doi:10.70675/1f03460cze5d6z42c6za18ez352e34a4dee4
Metadata
- Authors
- Wang, X., Belguise, K., Kersual, N., Kirsch, K. H., Mineva, N. D., Galtier, F., Chalbos, D., & Sonenshein, G. E.
- Affiliations
- Boston University (US)
- Inserm (FR)
- Corresponding author
- Sonenshein, Gail E.
- ORCID
- Venue
- Nature Cell Biology
- Published
- 2007-03-18
- Volume
- 9
- Issue
- 4
- Pages
- 470-478
- ISSN
- 1465-7392 (ISSN-L)
- 1476-4679
- PMC
- PMC2394707
- OpenAlex
- W2112528220
- Cited by
- 209
- References
- 37
- Citations by year
- 2026: 1 · 2025: 2 · 2024: 2 · 2023: 7 · 2022: 5 · 2021: 9 · 2020: 5 · 2019: 7 · 2018: 10 · 2017: 9 · 2016: 12 · 2015: 13 · 2014: 11 · 2013: 18 · 2012: 22
- FWCI
- 7.19
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature Cell Biology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- HAL (submittedVersion, other-oa)
- Funders
- National Cancer Institute (R01CA036355, CA 36355)
- National Institute of Environmental Health Sciences (ES 11624, P01ES011624)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › NF-κB Signaling Pathways
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Endocrinology › Estrogen and related hormone effects
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Signaling Pathways in Disease
- Keywords
- RelB, NF-κB, estrogen receptor alpha, breast cancer, tumor invasion, epithelial-mesenchymal transition, Bcl-2, c-Rel, transcriptional regulation
- MeSH terms
- Animals, Breast Neoplasms, Cell Movement, Cell Transformation, Neoplastic, Estrogens, Female, Humans, Microscopy, Fluorescence, Phenotype, Protein Binding, Immunoblotting, Blotting, Northern, Signal Transduction, Gene Expression Regulation, Neoplastic, NF-kappa B, Proto-Oncogene Proteins c-bcl-2, Reverse Transcriptase Polymerase Chain Reaction, Electrophoretic Mobility Shift Assay, Cell Line, Tumor, Estrogen Receptor alpha, Mice, Transcription Factor RelB, Fos-Related Antigen-2
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