Early studies documented the existence of sexual dimorphism in bladder cancer occurrence and progression, with a greater bladder cancer incidence in males than females. However, the progression of bladder cancer after diagnosis is much quicker in females than males. These findings can be explained by the effects of female hormones (predominantly oestrogens) and their binding receptors, including oestrogen receptor 1 (ESR1; also known as ERα), oestrogen receptor 2 (ESR2; also known as ERβ), and GPR30 protein on bladder cancer incidence and progression. Results from studies using various in vitro cell lines and in vivo mouse models demonstrate differential roles of oestrogen receptors in cancer initiation and progression. ERα suppresses bladder cancer initiation and invasion, whereas ERβ promotes bladder cancer initiation and progression. Mechanistic studies suggest that ERα and ERβ exert these effects via modulation of the AKT pathway and DNA replication complex, respectively. Targeting these signalling pathways--for example, with ERα agonists, ERβ antagonists, or selective oestrogen receptor modulators such as 4-[2-phenyl-5,7-bis(trifluoromethyl)pyrazolo[1,5-a]pyrimidin-3-yl]phenol (also known as PHTPP)--could lead to the development of new therapeutic approaches for controlling bladder cancer progression.