Epithelial ovarian cancer accounts for 1,300 new cases and 900 deaths each year, making it the most common cause of death among women with gynaecologic cancer. High-grade serous ovarian tumours (HGSOC) are characterised in part by their genomic instability, which leads to rapid progression to chemo-resistance in a majority of women. Recent anti-cancer therapy strategies aim to overcome the development of chemo-resistance by targeting stromal factors within the tumour microenvironment, which tumours rely on for progression and metastasis. Our study aims to characterise stromal factors that are upregulated in HGSOC as potential therapeutic targets. We analysed gene expression profiles from fibroblasts micro-dissected from HGSOC tumours and normal ovaries. We identified Connective Tissue Growth Factor (CTGF), a secreted protein that promotes proliferation and ECM production, as over-expressed specifically in HGSOC tumour fibroblasts. FG-3019, a human antibody against CTGF, is currently under clinical investigation in pancreatic cancer and fibrotic diseases. We performed functional studies to determine the potential of FG-3019 as a therapeutic agent in HGSOC. CTGF increased anchorage-independent growth and migration of ovarian cancer cell lines. During tumour progression, HGSOC cells from the ovary adhere to the peritoneum and disseminate throughout the peritoneal cavity, posing a major challenge in treatment. In ex-vivo peritoneal adhesion assays, CTGF increased adhesion of ovarian cancer cells to peritoneal tissue. CTGF-promoted migration and peritoneal adhesion were significantly inhibited by FG-3019. Our findings demonstrate that CTGF is over-expressed specifically in HGSOC tumour fibroblasts and increases the tumourigenicity of ovarian cancer cells. Furthermore, CTGF enhances adhesion of ovarian cancer cells to peritoneal tissue, suggesting that it may play a role in HGSOC metastasis. These effects of CTGF are blocked by FG-3019, a therapeutic monoclonal antibody currently under clinical investigation in pancreatic cancer. Our study suggests that CTGF may serve as a potential therapeutic target in HGSOC.