Given the task definition and input, reply with output. In this task, you are given an abstract of article. Your task is to generate title for this article. Preferred titles are under thirty words.

Transforming growth factor (TGF) is a potent and context-dependent regulator of tumor progression. TGF promotes the lung metastasis of basal-like (but not the luminal-like) breast cancer. Here, we demonstrated that fascin, a pro-metastasis actin bundling protein, was a direct target of the canonical TGF-Smad4 signaling pathway in basal-like breast cancer cells. TGF and Smad4 induced fascin overexpression by directly binding to a Smad binding element on the fascin promoter. We identified GATA3, a transcription factor crucial for mammary gland morphogenesis and luminal differentiation, as a negative regulator of TGF- and Smad4-induced fascin overexpression. When ectopically expressed in basal-like breast cancer cells, GATA-3 abrogated TGF- and Smad4-mediated overexpression of fascin and other TGF response genes, invadopodium formation, cell migration, and invasion, suggesting suppression of the canonical TGF-Smad signaling axis. Mechanistically, GATA3 abrogated the canonical TGF-Smad signaling by abolishing interactions between Smad4 and its DNA binding elements, potentially through physical interactions between the N-terminal of GATA3 and Smad3/4 proteins. Our findings provide mechanistic insight into how TGF-mediated cell motility and invasiveness are differentially regulated in breast cancer.
GATA3 transcription factor abrogates Smad4 transcription factor-mediated fascin overexpression, invadopodium formation, and breast cancer cell invasion.