SMAD2 and breast carcinoma: Thus, the presence or overexpression of LKB1 diminished the responses of breast cancer cells and precancerous mammary epithelial cells to TGF-β, leading to reduced phosphorylation of Smad2/3 and its transcription activity, whereas knockdown of LKB1 and AMPKα1 resulted in opposite changes and disruption of the acinus structure derived from mammary epithelial cells.