NDLI: Defective repression of c-myc in breast cancer cells: A loss at the core of the transforming growth factor beta growth arrest program.

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Defective repression of c-myc in breast cancer cells: A loss at the core of the transforming growth factor beta growth arrest program.

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Defective repression of c-myc in breast cancer cells: A loss at the core of the transforming growth factor beta growth arrest program.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Kang, Y. Massagué, J. Chen, C. R.
Description	Author Affiliation: Chen CR ( Cell Biology Program, Memorial Sloan-Kettering Cancer Center and Howard Hughes Medical Institute, New York, NY 10021, USA.);
Abstract	Loss of growth inhibitory responses to the cytokine transforming growth factor beta (TGF-beta) in cancer cells may result from mutational inactivation of TGF-beta receptors or their signal transducers, the Smad transcription factors. In breast cancer, however, loss of TGF-beta growth inhibition often occurs without a loss of these signaling components. A genome-wide analysis of rapid TGF-beta gene responses in MCF-10A human mammary epithelial cells and MDA-MB-231 breast cancer cells shows that c-myc repression, a response that is key to the TGF-beta program of cell cycle arrest, is selectively lost in the cancer cell line. Transformation of MCF-10A cells with c-Ha-ras and c-erbB2 oncogenes also led to a selective loss of c-myc repression and cell cycle arrest response. TGF-beta stimulation of epithelial cells rapidly induces the formation of a Smad complex that specifically recognizes a TGF-beta inhibitory element in the c-myc promoter. Formation of this complex is deficient in the oncogenically transformed breast cells. These results suggest that a Smad complex that specifically mediates c-myc repression is a target of oncogenic signals in breast cancer.
ISSN	00278424
e-ISSN	10916490
Journal	Proceedings of the National Academy of Sciences of the United States of America
Issue Number	3
Volume Number	98
Language	English
Publisher	National Academy of Sciences
Publisher Date	2001-02-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Breast Neoplasms Genetics Pathology Gene Expression Regulation, Neoplastic Gene Expression Regulation Genes, Myc Transforming Growth Factor Beta Pharmacology Breast Cell Cycle Drug Effects Epithelial Cells Cytology Physiology Molecular Sequence Data Proto-Oncogene Proteins C-myc Metabolism Transcription, Genetic Tumor Cells, Cultured Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, P.H.S. Multidisciplinary
Content Type	Text
Resource Type	Article
Subject	Multidisciplinary

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