Stimulation of endogenous FGFR2 signalling in MCF-7 cells following knock-down of FGFR2

Genome-wide association studies have identified a locus within the second intron of the FGFR2 gene that is consistently the most strongly associated with estrogen receptor-poisive breast cancer risk. However, we know little about the mechanisms by which the FGFR2 locus mediates risk or the pathways in which multiple risk loci may combine to cause disease. Previously, a systems biology approach was adopted to elucidate the regulatory networks operating in MCF-7 breast cancer cells in order to examine the role of FGFR2 in mediating risk. Here, the same approach has been employed using MCF-7 cells that have been treated with siRNA directed against FGFR2, in order to knock-down FGFR2 expression, to confirm that the differential gene expression that we see when FGF10 signalling is perturbed, on a background of estrogen signalling, is mediated via FGFR2 stimulation. The data consists of 24 microarray samples from MCF-7 cells treated under different conditions at a time point of 6 h in order to perturb FGFR2 signalling. The data have been pre-processed in R using the beadarray package, and are presented in the form of log2 expression values. The experiment was carried out on 2 Humanv4 arrays using 12 samples per array.