ArticlePloS one2013
Development of a reactive stroma associated with prostatic intraepithelial neoplasia in EAF2 deficient mice.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 26 citations in OpenAlex.
- EAF2 Downregulation Recruits Tumor-associated Macrophages in Prostate Cancer through Upregulation of MIF.Biological procedures online · 2024Article
- EAF2 loss induces prostatic intraepithelial neoplasia from luminal epithelial cells in mice.American journal of clinical and experimental urology · 2020Article
- Conditional Deletion of Eaf1 Induces Murine Prostatic Intraepithelial Neoplasia in Mice.Neoplasia (New York, N.Y.) · 2019Article
- Regulation of ELL2 stability and polyubiquitination by EAF2 in prostate cancer cells.The Prostate · 2018Article
- EAF2 and p53 Co-Regulate STAT3 Activation in Prostate Cancer.Neoplasia (New York, N.Y.) · 2018Article
- Concurrent EAF2 and ELL2 loss phenocopies individual EAF2 or ELL2 loss in prostate cancer cells and murine prostate.American journal of clinical and experimental urology · 2018Article
- Combined Loss of EAF2 and p53 Induces Prostate Carcinogenesis in Male Mice.Endocrinology · 2017Article
- Conditional deletion of ELL2 induces murine prostate intraepithelial neoplasia.The Journal of endocrinology · 2017Article
- EAF2 regulates DNA repair through Ku70/Ku80 in the prostate.Oncogene · 2017Article
- Regulation of tumor suppressor EAF2 polyubiquitination by ELL1 and SIAH2 in prostate cancer cells.Oncotarget · 2016Article
- EAF2 mediates germinal centre B-cell apoptosis to suppress excessive immune responses and prevent autoimmunity.Nature communications · 2016Article
Corrections and comments
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Authors and funding
17 authors at 5 institutions in 2 countries.
Funding
Abstract
ELL-associated factor 2 (EAF2) is an androgen-responsive tumor suppressor frequently deleted in advanced prostate cancer that functions as a transcription elongation factor of RNA Pol II through interaction with the ELL family proteins. EAF2 knockout mice on a 129P2/OLA-C57BL/6J background developed late-onset lung adenocarcinoma, hepatocellular carcinoma, B-cell lymphoma and high-grade prostatic intraepithelial neoplasia. In order to further characterize the role of EAF2 in the development of prostatic defects, the effects of EAF2 loss were compared in different murine strains. In the current study, aged EAF2(-/-) mice on both the C57BL/6J and FVB/NJ backgrounds exhibited mPIN lesions as previously reported on a 129P2/OLA-C57BL/6J background. In contrast to the 129P2/OLA-C57BL/6J mixed genetic background, the mPIN lesions in C57BL/6J and FVB/NJ EAF2(-/-) mice were associated with stromal defects characteristic of a reactive stroma and a statistically significant increase in prostate microvessel density. Stromal inflammation and increased microvessel density was evident in EAF2-deficient mice on a pure C57BL/6J background at an early age and preceded the development of the histologic epithelial hyperplasia and neoplasia found in the prostates of older EAF2(-/-) animals. Mice deficient in EAF2 had an increased recovery rate and a decreased overall response to the effects of androgen deprivation. EAF2 expression in human cancer was significantly down-regulated and microvessel density was significantly increased compared to matched normal prostate tissue; furthermore EAF2 expression was negatively correlated with microvessel density. These results suggest that the EAF2 knockout mouse on the C57BL/6J and FVB/NJ genetic backgrounds provides a model of PIN lesions associated with an altered prostate microvasculature and reactive stromal compartment corresponding to that reported in human prostate tumors.
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