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[Cancer Research 63, 8284-8292, December 1, 2003]
© 2003 American Association for Cancer Research

Regular Articles

Reduction in Smad2/3 Signaling Enhances Tumorigenesis but Suppresses Metastasis of Breast Cancer Cell Lines

Fang Tian, Stacey DaCosta Byfield, W. Tony Parks, Stephen Yoo, Angelina Felici, Binwu Tang, Ester Piek, Lalage M. Wakefield and Anita B. Roberts

Laboratory of Cell Regulation and Carcinogenesis, National Cancer Institute, Bethesda, Maryland

The role of transforming growth factor ß in breast cancer is controversial with tumor suppressor and pro-oncogenic activities having been demonstrated. To address whether the same or different signal transduction pathways mediate these opposing activities, we manipulated the Smad2/3 signaling pathway in cells of common origin but differing degrees of malignancy derived from MCF10A human breast cells. We show that interference with endogenous Smad2/3 signaling enhances the malignancy of xenografted tumors of premalignant and well-differentiated tumor cells but strongly suppresses lung metastases of more aggressive carcinoma cells after tail vein injection. Overexpression of Smad3 in the same cells has opposite effects. The data demonstrate that the Smad2/3 signaling pathway mediates tumor suppressor and prometastatic signals, depending on the cellular context.




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Molecular Cancer Research Cancer Prevention Research
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Copyright © 2003 by the American Association for Cancer Research.