In previous studies we showed that PRH overexpression in MDA-MB-231 breast cancer cells also inhibits cell migration and significantly reduces the ability of these cells to invade Matrigel in vitro.12 We have shown here that inducible knockdown of PRH in MCF-7 breast tumour cells results in additional tumorigenic properties including increased cell proliferation, due in part to increased expression of cell cycle genes, to increased autocrine VEGF signalling through VEGFA and most likely VEGFC, and increased mammosphere forming frequency. This evidence concerns the gene VEGFA and breast carcinoma.