{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,11,11]],"date-time":"2025-11-11T22:04:35Z","timestamp":1762898675118},"reference-count":47,"publisher":"Wiley","issue":"15","license":[{"start":{"date-parts":[[2011,3,28]],"date-time":"2011-03-28T00:00:00Z","timestamp":1301270400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["The Prostate"],"published-print":{"date-parts":[[2011,11]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>BACKGROUND<\/jats:title><jats:p>Despite dramatic positive effects, there is evidence that the androgen receptor (AR) may negatively influence prostate tumor progression. Understanding the AR repressor function and how it is subverted is of particular importance in anti\u2010androgen and AR intervention strategies.<\/jats:p><\/jats:sec><jats:sec><jats:title>METHODS<\/jats:title><jats:p>AR, resident FGFR2IIIb, and ectopic FGFR1 were expressed by transfection in the AR\u2010negative epithelial cell line DTE that predominates in cell culture of AR\u2010positive androgen\u2010responsive model Dunning R3327 rat prostate tumors. Androgen\u2010responsiveness at transcription was measured by a luciferase reporter. Cell population growth rates were assessed by cell counts, DNA synthesis, and expression of cell cycle genes. AR variants (ARVs) were assessed by immunochemistry and nuclease protection of mRNA.<\/jats:p><\/jats:sec><jats:sec><jats:title>RESULTS<\/jats:title><jats:p>Expression of AR inhibited cell population growth of AR\u2010negative DTE cells at the G1\u2013S phase of the cell cycle. Ectopic FGFR1, but not resident FGFR2IIIb abrogated the growth inhibitory effects of AR. Appearance of ARVs was coincident with co\u2010expression of FGFR1 and AR and abrogation of the AR\u2010dependent inhibition of cell growth.<\/jats:p><\/jats:sec><jats:sec><jats:title>CONCLUSIONS<\/jats:title><jats:p>DTE cells may represent non\u2010malignant AR\u2010negative progenitors whose population is restricted by activation of AR in vivo. Ectopic expression of epithelial FGFR1, a common observation in tumors, overrides the inhibition of AR and thus may contribute to evolution of androgen and AR independent tumors. These results are consistent with the notion that some tumor cells are negatively restricted by AR and are unleased by androgen\u2010deprivation or ectopic expression of FGFR1. ARV's may play a role in the bypass of the negative restrictions of AR. Prostate 71:1691\u20131700, 2011. \u00a9 2011 Wiley\u2010Liss, Inc.<\/jats:p><\/jats:sec>","DOI":"10.1002\/pros.21386","type":"journal-article","created":{"date-parts":[[2011,3,28]],"date-time":"2011-03-28T21:57:42Z","timestamp":1301349462000},"page":"1691-1700","source":"Crossref","is-referenced-by-count":3,"title":["FGFR1 abrogates inhibitory effect of androgen receptor concurrent with induction of androgen\u2010receptor variants in androgen receptor\u2010negative prostate tumor epithelial 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