The knockdownof Smad3 in MDA-MB-231 cells resulted in the prolonged latency and delayedgrowth of metastases, whereas Smad2 knockdown resulted in a more aggressivephenotype compared with control cells.9Therefore, we demonstrated that Bcl-3 serves as a critical regulator instabilizing Smad3, but not Smad2 or Smad4, upon TGFβ stimulation.This function is crucial for the TGFβ-dependent cell migration,invasion and pulmonary metastasis of breast cancer. This evidence concerns the gene SMAD2 and breast carcinoma.