Combined PI3K/ERα inhibition attenuates effects of obesity on breast cancer cell viability and growth. The contribution of the PI3K/Akt, MAPK, and ERα pathways to obese (Ob) patient sera-induced cell viability and growth was examined via treatment of MCF-7 cells with the following inhibitors during sera exposure: LY 294,002 (LY, a PI3K inhibitor, 10uM), PD 98,059 (PD, a MEK1 inhibitor, 10uM) and 4-hydroxytamoxifen (Tam, a selective estrogen receptor modulator, 100 nM). (A) MCF-7 cell viability was measured by MTT assay following a 48 hour exposure to 2% Ob or control (Con) patient sera, with or without drug treatment. (B) Colony formation assay was used to assess MCF-7 cell growth over a nine day exposure to 2% Ob or Con patient sera, with or without drug treatment. Data shown represent the average of at least three independent experiments, and different letters indicate significant differences (P < 0.05). ERα, estrogen receptor alpha; MTT reagent, 3-(4,5-dmethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide.