Credit: © R.W. Jones/CORBIS

As well as being important regulators of developmental and physiological processes, steroid hormones have a darker side — in the development and progression of breast, ovarian and prostate cancer. This was believed to be due to stimulation of proliferation, but evidence presented by Jianwu Bai and colleagues in Cell suggests a new function for steroid hormones: making cells move.

Using the Drosophila melanogaster egg chamber, this group has identified mutants that block movement towards the oocyte of a group of cells called border cells. Genes previously identified using this system include slow border cells ( slbo ), which encodes a transcription factor, and the Drosophila E-cadherin gene. Their latest screen has identified taiman ( tai ) — meaning 'too slow': mutant clones typically remain stuck at the anterior end of the egg chamber instead of moving towards the oocyte. tai mutants had normal expression levels of SLBO, indicating that TAI might be involved in a different pathway from SLBO, but E-cadherin was mislocalized.

So what is TAI? It turns out to belong to a family of steroid-receptor co-activator (SRC) proteins previously not thought to exist in Drosophila. Its closest relative in mammals is AIB1, a SRC that is amplified in breast and ovarian cancer. Which steroid hormone receptor does TAI interact with? Several genes for steroid hormone receptors have been identified in the Drosophila genome but only one of these, the ecdysone receptor (a hetrodimer of the USP and EcR proteins), has a known ligand, which is synthesized by the ovary. USP and EcR were expressed together with TAI in wild-type border cells and TAI, USP and EcR colocalized exactly on Drosophila polytene chromosomes, indicating that the three proteins form a complex. Furthermore, provided that SLBO was also expressed, treatment with ecdysone caused precocious migration of border cells whereas migration was abrograted in an ecdysoneless mutant.

What next? As well as identifying the targets of the ecdysone receptor–taiman complex, it will be important to determine whether AIB1 has similar effects on cell motility in vertebrates. If so, it could explain the increased invasiveness of AIB1-overexpressing cancer cells and suggest new therapeutic avenues.