A new study has reported that estrogen and insulin-like growth factor (IGF) promote breast cancer together and independently by inhibiting cellular processes designed to repress breast cancer growth. The study was designed to investigate the interactions between estrogen and IGF signaling in breast cancer. While both estrogen receptor (ER) and IGF-like growth factor signaling are known to be important for breast cancer, as well as for normal breast development, interaction between these pathways is not well understood.

To conduct the study, the authors performed microarray analysis to determine gene expression in hormone receptor positive MCF-7 breast cancer cells treated with estradiol (E2) or IGF-I for either three or 24 hours.

Each gene encodes a unique protein that performs a specialized function in cells. Cells use a two-step process of transcription and translation to read the gene and produce its protein. Gene transcription is the process by which genetic information is copied from DNA to RNA. This is followed by translation, in which the RNA is read and a specific protein is produced. IGF-I was found to regulate the RNA of five to ten times as many genes as E2. Many genes were co-regulated by both. Of significance was that expression of co-regulated genes correlated with poor breast cancer prognosis. Importantly, the expression of number of potential tumor suppressors was inhibited by IGF-I and E2. Analysis of three such down-regulated genes demonstrated that they were repressed either by E2 or IGF but not both. However, other study results suggested downstream convergence of the two pathways. The authors conclude that E2 and IGF-I co-regulate a set of genes that influence breast cancer outcome. Effective treatment of tumors with active ER and IGF signaling may require co-targeting of both pathways.