Skip to main content
. Author manuscript; available in PMC: 2014 Apr 16.
Published in final edited form as: Cell Rep. 2014 Mar 13;6(6):1000–1007. doi: 10.1016/j.celrep.2014.02.023

Figure 1. miR-34 and p53 Cooperate in Suppression of Prostate Carcinogenesis.

Figure 1

(A, B) Quantitative analysis of frequency of neoplastic lesions in proximal (A) and distal (B) regions of prostatic ducts. N: normal, PRD: proximal dysplastic lesions, AC: adenocarcinoma, LG: LG PIN, HG: HG PIN. (C) Proximal (left two columns) and distal (right two columns) regions of prostatic ducts in 15-month-old wild-type (WT) and p53PE−/−mir-34PE−/− mice. Adenocarcinomas invading surrounding stroma (arrows) and filling up the lumen (arrowheads) in the proximal regions of prostatic ducts of p53PE−/−mir-34PE−/− mice. PIN4 (arrows) in the distal regions of prostatic ducts of p53PE−/−mir-34PE−/− mice. As compared to the prostate epithelium of WT mice, both adenocarcinomas and PIN4 (arrows) show higher expression levels of AMACR and EZH2 and increased number of CK5 and p63 positive cells. Hematoxylin and eosin (HE images). ABC Elite method with hematoxylin (AMACR, CK5) or methyl green (EZH2, and p63) counterstaining. Scale bar, 100 μm for all images. (D, E) Quantitative analysis of proliferation rate in proximal (D) and distal (E) regions of prostatic ducts. *P<0.05, **P<0.01. Error bars denote SD. See also Figure S3A.

HHS Vulnerability Disclosure