ArticleCell cycle (Georgetown, Tex.)2017
p16 loss rescues functional decline of Brca1-deficient mammary stem cells.
Article in Cell cycle (Georgetown, Tex.), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 22 citations in OpenAlex.
- BRCA1 heterozygosity promotes DNA damage-induced senescence in a sex-specific manner following repeated mild traumatic brain injury.Frontiers in neuroscience · 2023Article
- PDGFRβ is an essential therapeutic target for BRCA1-deficient mammary tumors.Breast cancer research : BCR · 2021Article
- Breast cancer type 1 and neurodegeneration: consequences of deficient DNA repair.Brain communications · 2021Review
- GATA3 functions downstream of BRCA1 to suppress EMT in breast cancer.Theranostics · 2021Article
- Aggressiveness Potential of Spontaneous Canine Mucosal Melanoma Can Dictate Distinct Cancer Stem Cell Compartment Behaviors in Regard to Their Initial Size and Expansion Abilities.Stem cells and development · 2020Article
- BRCA1 Attenuates Progesterone Effects on Proliferation and NFκB Activation in Normal Human Mammary Epithelial Cells.Journal of mammary gland biology and neoplasia · 2019Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Recent evidence indicates that the accumulation of endogenous DNA damage can induce senescence and limit the function of adult stem cells. It remains elusive whether deficiency in DNA damage repair is associated with the functional alteration of mammary stem cells. In this article, we reported that senescence was induced in mammary epithelial cells during aging along with increased expression of p16Ink4a (p16), an inhibitor of CDK4 and CKD6. Loss of p16 abrogated the age-induced senescence in mammary epithelial cells and significantly increased mammary stem cell function. We showed that loss of Brca1, a tumor suppressor that functions in DNA damage repair, in the mammary epithelium induced senescence with induction of p16 and a decline of stem cell function, which was rescued by p16 loss. These data not only answer the question as to whether deficiency in DNA damage repair is associated with the functional decline of mammary stem cells, but also identify the role of p16 in suppressing Brca1-deficient mammary stem cell function.
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Registered trials
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