Constitutive activation of RANK disrupts mammary cell fate leading to tumorigenesis
Abstract
Receptor Activator of NF-kappa B (RANK) pathway controls mammary gland development in mice but its role in mammary stem cell fate remains undefined. We show that constitutive RANK signaling expands luminal and basal mammary compartments including mammary stem and luminal progenitor cell pools and interferes with the generation of CD61+ and Sca1+ luminal cells and Elf5 expression. Impaired mammary cell commitment upon RANK overexpression leads to the accumulation of progenitors including K14+K8+ bipotent cells and the formation of heterogeneous tumors containing hyperplastic basal, luminal, and progenitor cells. RANK expression increases in wild-type mammary epithelia with age and parity, and spontaneous preneoplastic lesions express RANK and accumulate K14+K8+ cells. In human breast tumors, high RANK expression levels are also associated with altered mammary differentiation. These results suggest that increased RANK signaling interferes with mammary cell commitment, contributing to breast carcinogenesis.
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TNFRSF11A expression increases during ageing, leading to DNA damage and senescence through Cdkn2a.
“The expression of TNFRSF11A increases during ageing228, leading to DNA damage and senescence through Cdkn2a (ref. 229).”
From SenNet recommendations for detecting senescent cells in different tissues (2024) · cites this paper as [228]
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- Authors
- Pellegrini, P., Cordero, A., Gallego, M. I., Dougall, W. C., Purificación, M., Pujana, M. A., & Gonzalez-Suarez, E.
- Affiliations
- Institut d'Investigació Biomédica de Bellvitge (ES)
- Cancer Epigenetics and Biology Program Bellvitge Biomedical Research Institute, IDIBELL, Barcelona, Spain
- Instituto de Salud Carlos III (ES)
- Amgen (United States) (US)
- Translational Research Laboratory, Breast Cancer Unit Catalan Institute of Oncology, Bellvitge Biomedical Research Institute, IDIBELL, Barcelona, Spain
- Venue
- Stem Cells
- Publisher
- Oxford University Press (OUP)
- Published
- 2013-09-01
- Volume
- 31
- Issue
- 9
- Pages
- 1954-1965
- ISSN
- 1066-5099 (ISSN-L)
- 1549-4918
- OpenAlex
- W1512180952
- Cited by
- 52
- References
- 40
- Citations by year
- 2026: 3 · 2025: 3 · 2024: 3 · 2023: 7 · 2022: 3 · 2021: 4 · 2020: 3 · 2019: 3 · 2018: 2 · 2017: 4 · 2016: 7 · 2015: 6 · 2014: 3 · 2013: 1
- FWCI
- 3.03
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- academic.oup.com/journals/pages/open_access/funder_policies/chorus/standard_publication_model (vor)
- Locations
- Stem Cells (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Oncology › Cancer Cells and Metastasis
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Developmental Biology and Gene Regulation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › NF-κB Signaling Pathways
- Keywords
- RANK signaling, mammary stem cells, mammary gland development, luminal progenitor cells, basal progenitor cells, ELF5, CD61, spinocerebellar ataxia type 1, mammary gland hyperplasia, precancerous lesions, mammary carcinogenesis, mammary gland differentiation, NF-κB
- MeSH terms
- Adenocarcinoma, Aging, Animals, Breast Neoplasms, Cell Compartmentation, Cell Differentiation, Epithelium, Female, Humans, Keratins, Mammary Glands, Animal, Mammary Tumor Virus, Mouse, Mammary Neoplasms, Experimental, Models, Biological, Parity, Precancerous Conditions, Pregnancy, Stem Cells, Gene Expression Regulation, Neoplastic, Cell Lineage, Cell Shape, Mice, Receptor Activator of Nuclear Factor-kappa B, Carcinogenesis
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