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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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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