17 β-Estradiol (E2) and its metabolites differentially activate PI3K/AKT signaling pathway during mammary transformation.

<p>A. Estrogen-induced PI3K phosphotylation. B. Estrogen-induced AKT phosphotylation. MCF-10A cells were exposed to a carcinogenic regimen of E2 and its metabolites – 2-OH-E2 or 4-OH-E2 as described in the legend of <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0054206#pone-0054206-g002" target="_blank">figure 2</a>. At the end of transformation process, cells were treated for additional 30 minutes with E2, 2-OH-E2 or 4-OH-E2, respectively. The cellular extracts from treated and controls cells were immuno-precipitated with PI3K or AKT specific monoclonal antibodies and followed by Western detection of PI3K or AKT phosphorylation using phosphor-threonine antibody. Results are expressed as mean fold change of three separate experiments. *P<0.05, significantly different from contol. **P<0.001 indicates significantly different from control.