AI Article Synopsis
- Pten deletion in adult prostatic epithelial cells leads to increased cell growth and the development of prostatic intraepithelial neoplasia (PIN) in mice.
- The study reveals that Pten-deficient cells experience replication stress and trigger a DNA damage response.
- This response ultimately results in cell senescence, similar to what occurs in cells influenced by oncogenes.
Article Abstract
We report that Pten (phosphatase and tensin homologue) ablation in prostatic epithelial cells of adult mice promotes cell proliferation to generate prostatic intraepithelial neoplasia. Moreover, our results demonstrate that proliferating Pten-deficient cells undergo replication stress and exhibit a DNA damage response, leading to cell senescence, as seen in oncogene-induced senescence.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6370383 | PMC |
| http://dx.doi.org/10.1080/23723556.2018.1511205 | DOI Listing |
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