Epigenetic silencing of individual tumour suppressor genes is a common signature of cancer and can affect multiple genes in one cancer cell. The mechanisms of epigenetically mediated inactivation of genes and regions during carcinogenesis have yet to be fully elucidated. The role of long non-coding RNA (lncRNA) transcripts in directing epigenetic remodeling of genes in cancer is poorly understood. Particularly, the targeting of specific regions of the genome by PRC2, a process that we and others hypothesise may be guided by lncRNA molecules. We characterised PRC2 binding of lncRNAs on a genome wide basis in cancer cells using RNA Immunoprecipitation (RIP) of RNA bound to the EZH2 subunit of the PRC2 complex in both PrEC (normal prostate) and LNCaP (prostate cancer cell line), coupled with Illumina sequencing and hybridisation to microarrays (Affymetrix 2.0ST Gene Array). Differences in transcript abundance between PrEC and LNCaP cells were assayed by strand-specific RNA-Seq and HuGene Affy Arrays. Methods to process these RIP-Seq and RNA-seq datasets are freely available as implemented in NGSANE --a publically available Analysis Framework for Biological Data from High Throughput Experiments. We present our current findings and comparisons using these high-throughput approaches to elucidate the polycomb bound transcriptome in both LNCaP and PrEC cells that may mediate remodeling of the cancer epigenome.