Since its discovery in the late 1970s considerable research has linked transforming growth factor-beta (TGF-beta) to several human diseases such as fibrosis, auto-immunity and cancer. TGF-beta acts initially as a growth inhibitory factor in early stages of tumour development. In contrast, as tumours evolve, they develop mechanisms to evade the growth-regulatory effects of TGF-beta, resulting in greater tumour invasiveness, increased metastatic potential and inhibition of surrounding immune responses. However, although extensively studied, the molecular mechanisms that trigger tumour cells to "switch" from TGF-beta-inhibited to TGF-beta-promoted are still not fully understood. Contradictory studies that demonstrate opposite cellular effects mediated by TGF-beta are abundant throughout the literature. This review summarizes the current molecular mechanisms involved in the tumour suppressive and tumour progressive characteristics of TGF-beta in brain tumours. Potential therapeutic agents that target TGF-beta and related proteins being evaluated against brain tumours is also discussed.