Ovarian cancer remains one of the deadliest female gynaecological cancers affecting 314,000 women and attributing to 207,000 deaths worldwide. The most common type of ovarian cancer, epithelial ovarian cancer (EOC), is a highly aggressive cancer of unmet clinical need, and novel treatment options are urgently needed for EOC patients due to the ability of the tumour to become resistant to cytotoxic drugs resulting in tumour recurrence. The fibroblast growth factor receptor 1 (FGFR1) is an important regulator of signalling pathways associated with proliferation and cell migration and has been found to be a driver of such activities in many cancers; FGFR1 mutations have been recently reported in EOC and as such this receptor may be a novel target to improve patients’ outcome. Preliminary data had suggested that FGFR1 is involved in EOC cell migration, here these initial observations were investigated employing various migration studies in vitro. Migratory activities were investigated by 2D scratch and 3D invasion assays, targeting cell migration and invasion using three selected and engineered EOC cell lines, 1847scr, 1487 FGFR1 kd (HGSC) and A2780 (endometroid) with a panel of FGFR specific inhibitors. In addition, FGFR1 levels (both total and activated) were determined for the cell lines under unstimulated and FGF2 ligand stimulated conditions. The results showed firstly that morphologically the 1847 cell line, after stable knockdown of FGFR1 exhibited enhanced epithelial-like features in comparison to the more mesenchymal-like FGFR1 scramble control. The third cell line, A2780, displayed only epithelial-like, cobble stone features with close associations between cells. Analysis of total and phosphorylated levels of FGFR1 highlighted striking differences with A2780 displaying the lowest protein levels (p