AI Article Synopsis
- The mammary epithelium undergoes significant growth during the female reproductive cycle, driven by mammary stem cells that can self-renew.
- This growth process needs to be carefully controlled to avoid tumor development, with tumor suppressors p53, p16, and p19 known to play a role in regulating this balance.
- Research using specific mouse models shows that p53, p16, and p19 do not significantly restrict normal mammary epithelial self-renewal and proliferation, but their presence can lead to increased cell growth when combined with the inflammatory cytokine TNF-α.
Article Abstract
The mammary epithelium undergoes several rounds of extensive proliferation during the female reproductive cycle. Its expansion is a tightly regulated process, fueled by the mammary stem cells and these cells' unique property of self-renewal. Sufficient new cells have to be produced to maintain the integrity of a tissue, but excessive proliferation resulting in tumorigenesis needs to be prevented. Three well-known tumor suppressors, p53, p16, and p19, have been connected to the limiting of stem cell self-renewal and proliferation. Here we investigate the roles of these three proteins in the regulation of self-renewal and proliferation of mammary epithelial cells. Using mammary epithelial-specific mouse models targeting Trp53 and Cdkn2a, the gene coding for p16 and p19, we demonstrate that p53, p16, and p19 do not play a significant role in the limitation of normal mammary epithelium self-renewal and proliferation, whereas in the presence of the inflammatory cytokine TNF-α, Trp53Cdkn2a mammary basal cells exhibit amplified proliferation.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7878826 | PMC |
| http://dx.doi.org/10.1016/j.stemcr.2020.12.012 | DOI Listing |
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