Fig. 3 : MME deficiency promotes aggressiveness of prostate carcinomas occurring in PtenPE−/− cells after castration. | Oncogenesis

Fig. 3 : MME deficiency promotes aggressiveness of prostate carcinomas occurring in PtenPE−/− cells after castration.

From: Membrane metalloendopeptidase suppresses prostate carcinogenesis by attenuating effects of gastrin-releasing peptide on stem/progenitor cells

Fig. 3

a Distal regions of prostatic ducts in 16-month-old PtenPE−/− (n = 6) and Mme−/−PtenPE−/− (n = 8) mice 8 months after castration. The arrows indicate positive immunostained cells. As compared to the prostate epithelium of PtenPE−/− mice, adenocarcinomas of Mme−/−PtenPE−/− mice show higher expression levels of MET, lowered expression of E-Cadherin (ECAD), and no change in AR expression. Increased number and proliferation rate of SYP-positive clusters. Immunostaining (b) and quantitative analysis of the frequency of SYP-positive clusters (c), and SYP cells expressing Ki67 therein (d) in distal regions of prostatic ducts. HE hematoxylin and eosin staining. The ABC Elite method with hematoxylin (MET, ECAD, and SYP) or methyl green (AR) counterstaining was performed. Double immunofluorescence with SYP (green) and Ki67 (red) with DAPI (blue) counterstaining. Scale bar, 60 µm for HE and all immunoperoxidase images, and 30 µm for fluorescence images. c, d P < 0.01. Error bars denote SD. All results are representative of six mice per genotype.

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