Long non-coding RNA (lncRNA) genes are abundant in the human genome and many are recognised to have oncogenic or tumour suppressor properties. We previously characterised the structure of GHRLOS, a gene situated on the opposite strand of the multifunctional peptide hormone ghrelin gene (GHRL), however, its expression and function in disease haven't been described. Here, interrogating The Cancer Genome Atlas (TCGA), we first revealed that GHRLOS is differentially expressed in a number of cancers and in particular, expression was elevated in endometrial and prostate cancer compared to normal tissues. Using qRT-PCR (and commercial cDNA panels) we confirmed that GHRLOS expression is upregulated in endometrial and prostate cancer. Forced GHRLOS overexpression did not significantly regulate the expression of the overlapping GHRL gene. GHRLOS overexpression significantly increased in vitro migration and proliferation of the PC3 metastatic prostate cancer cell line. In agreement, there was an increase in tumour volume (1.43-fold, unpaired t-test P < 0.0001) and expression of the cell proliferation marker Ki67 (1.25-fold, unpaired t-test P < 0.0001) in GHRLOS-overexpressing PC3 xenografts (n=12) grown subcutaneously in NOD/SCID mice. Associated genome-wide gene expression profiling revealed differential expression of 223 genes, including repression of ATM (-3.3-fold, moderated t-test Q=8.2×10-3), a master regulator of DNA repair and tumour suppressor frequently mutated in metastatic prostate cancer. The long non-coding RNAs MALAT1 (-8.0-fold, Q=6.0×10-3) and NEAT1 (-9.0-fold, Q=7.8×10-3) were also regulated by GHRLOS. Taken together, we show that the lncRNA GHRLOS is overexpressed in prostate cancer and may facilitate PC3 prostate cancer cell growth and migration in vitro, PC3 xenograft growth in vivo, and inhibit invasion by downregulating key associated non-coding RNAs. Ongoing studies aim to identify mechanisms used by this lncRNA to facilitate the functional effects observed.