Several studies have correlated escape from TGF‐β‐mediated cell cycle arrest with the tumorigenic phenotype. Most often, this escape from growth control has been linked to dysfunctional TGF‐β receptors or defects in the TGF‐β‐mediated SMAD signaling pathway. In this report, we found that highly metastatic 4T1 mammary carcinoma cells express functional TGF‐β receptors capable of initiating SMAD‐mediated transcription, yet are not growth inhibited by TGF‐β1. We further observed that TGF‐β directly contributes to the metastatic behavior of this cell line. Exposure to TGF‐β caused 4T1 cells to undergo morphological changes associated with the metastatic phenotype and invade more readily through collagen coated matrices. Furthermore, expression of a dominant negative truncated type II receptor diminished TGF‐β signaling and significantly restricted the ability of 4T1 cells to establish distant metastases. Our results suggest that regardless of 4T1 resistance to TGF‐β‐mediated growth inhibition, TGF‐β signaling is required for tumor invasion and metastases formation. Int. J. Cancer 91:76–82, 2001. © 2001 Wiley‐Liss, Inc.