Fig. 1: Deletion of AR in Gli1-expressing cells in the UGM impairs UGE oncogenic xenograft growth. | Nature Communications

Fig. 1: Deletion of AR in Gli1-expressing cells in the UGM impairs UGE oncogenic xenograft growth.

From: Stromal androgen signaling acts as tumor niches to drive prostatic basal epithelial progenitor-initiated oncogenesis

Fig. 1

a Schematic of the experimental timeline for tissue recombination and kidney capsule transplantation. Urogenital sinus epithelium (UGE) from Ctnnb1L(ex3)/+:PBCre4 embryos and urogenital sinus mesenchyme (UGM) from Gli1CreER/+ or ArL/Y:Gli1CreER/+ embryos after activation of Gli1CreER/+ are recombined and grown under the renal capsule of host mice. DOC, day of conception; TM, tamoxifen; KCT, kidney capsule transplantation. b Weights of xenograft recombinants from the indicated UGE and UGM combinations (left panel). Quantification of the percentage of Ki67+ cells per total cells (right panel). Data are represented as mean ± SD of five biological replicates. Two-sided Student’s t test, *p < 0.05, **p < 0.01. Source data and the exact p-values are provided as a Source Data file. cl Representative gross (cd, hi), hematoxylin-eosin (H&E) (e, j), and immunohistochemistry (IHC) for β-catenin (β-cat) and androgen receptor (AR) (fg, kl) images of xenograft tissues from the indicated UGE and UGM combinations. Scale bars, 2 mm (cd, hi), 100 μm (e, j), and 20 μm (fg, kl). The nuclear expression of β-cat in the epithelium is indicated by red arrows. Pink and blue arrows indicate epithelial and stromal AR+ cells, respectively.

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