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. Author manuscript; available in PMC: 2011 Jun 11.
Published in final edited form as: Mol Cell. 2010 Jun 11;38(5):662–674. doi: 10.1016/j.molcel.2010.03.021

Figure 1. Non-coding RNA ANRIL is Up-regulated in Prostate Cancer Tissues and Coincides with CBX7 and EZH2 Expression.

Figure 1

a, Schematic representation of the genomic organization of the INK4a/ARF gene cluster. Three genes in the INK4a/ARF locus are color-coded. Transcripts antisense to ANRIL (blue) used to inhibit ANRIL interactions (see Figure 2) are indicated above ANRIL. Roman numerals denote sites of quantitative ChIP as shown in Figure 3. b, Normalized expression levels of ANRIL, p16, CBX7 and EZH2 in normal prostate epithelium cells, and preneoplastic PIN and PCa prostate cancer cells. Each plotted point represents a separate tissue sample. c, Levels of ANRIL transcript relative to HPRT as detected in normal prostate epithelium and PC3 prostate cancer cells. d, RNA-FISH (fluorescence in situ hybridization) of ANRIL as detected in normal prostate and prostate cancer (PCa) cells. The housekeeping genes GAPDH and HPRT are shown as input controls. e, Relative enrichment of RNA polymerase II, EZH2 and CBX7 associated with loci spanning the INK4a/ARF region in the IMR90 fibroblasts (red) or PC3 prostate carcinoma (green) background. Standard ChIP analysis was performed at selected points overlapping transcript starts identified within the UCSC Genome Browser (chr9: 21,710,518-2,301,141), based on RefSeq, Uniprot, GeneBank, CCDS, and Comparative Genomics and plotted using Genome Graphs (http://genome.ucsc.edu). ChIP primers used are listed in Table S2. See also Figure S1.