ATP-dependent chromatin remodelling is required for all aspects of chromatin biology including transcription, DNA repair, DNA replication, and cell cycle progression. Deregulation of SMARCA4 (BRG1), an essential catalytic subunit of the SWI/SNF chromatin-remodelling complex, contributes to a wide range of malignancies. Furthermore, clinical studies have revealed that BRG1 is over expressed in prostate cancer and positively correlated with disease progression and invasiveness. However, the mechanisms underlying the involvement of BRG1 are unknown. Here we investigated the consequences of BRG1-depletion on the epigenome in LNCaP prostate cancer cells. BRG1 is over expressed in LNCAP cells compared to normal prostate epithelial cells (PrEC) and therefore provides an ideal model for molecular investigation. We found that BRG1 (ChIPseq) binding is enriched at active DNA regulatory elements including enhancers and promoters. Depletion of BRG1 causes a rapid compaction of chromatin (ATACseq) at active enhancers and at Polycomb marked regions, but not at promoters. This occurs concomitant with a reduction in H3K27ac and H3K4me1 (ChIPseq) leading to a significant reduction in the number of active enhancers. Despite the substantial effect on the enhancer landscape, we detected only a modest effect on gene expression (RNAseq), suggesting that vigorous compensatory mechanisms exist. The majority of gene expression changes were down regulated genes enriched for GO terms including cell cycle, DNA replication and DNA metabolism. Complementary FACS cell cycle analysis and determined that BRG1 loss reduces the number of cells in S-phase and increases cells in G1, corresponding with a reduction in proliferation. Taken together we find that BRG1 has a crucial role in maintaining open chromatin at active enhancers, which likely underpins the atypical gene expression signature and altered growth capacity of prostate cancer cells.