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Responsiveness to Transforming Growth Factor-β (TGF-β)-Mediated Growth Inhibition Is a Function of Membrane-Bound TGF-β Type II Receptor in Human Breast Cancer Cells

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Transforming growth factor-β (TGF-β) is a potent inhibitor of growth and proliferation of breast epithelial cells, and loss of sensitivity to its effects has been associated with malignant transformation and tumorigenesis. The biological effects of TGF-β are mediated by the TGF-β receptor complex, a multimer composed of TGF-β receptor type I (TβR-I) and TGF-β receptor type II (TβR-II) subunits. Evidence suggests that loss of expression of TβR-II is implicated in the loss of sensitivity of tumorigenic breast cell lines to TGF-β-mediated growth inhibition. A panel of human breast cell lines, including the immortalized MCF-10F and tumorigenic MCF-7, ZR75-1, BT474, T47-D, MDA-MB231, BT20, and SKBR-3 cell lines, was characterized for responsiveness to TGF-β-induced G1 growth arrest. Only the nontumorigenic MCF-10F and the tumorigenic MDA-MB231 cell lines demonstrated a significant inhibitory response to TGF-β1 and a significant binding of 125I-labeled TGF-β ligand. While expression of TβR-I mRNA was similar across the panel of cell lines, TβR-II mRNA expression was decreased significantly in all seven tumorigenic cell lines in comparison with the nontumorigenic MCF-10F cell line. When total cellular protein was fractionated by centrifugation, TβR-I protein was observed in both the cytosolic and membrane fractions at similar levels in all cell lines; however, TβR-II protein was present in the cytosolic fraction in all cell lines, but was observed in the membrane fraction of only the TGF-β-responsive MCF-10F and MDA-MB231 cells. Thus, lack of membrane-bound TβR-II protein appears to be an important determinant of resistance to TGF-β-mediated growth inhibition in this group of breast cell lines.
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Keywords: Breast cancer Transforming growth factor-β Transforming growth factor-β receptors Growth inhibition

Document Type: Research Article

Affiliations: 1: *Division of Environmental Health Sciences, School of Public Health, College of Medicine and Public Health, The Ohio State University, Columbus, OH 43210 2: †Department of Medicinal Chemistry and Pharmacognosy, College of Pharmacy, The Ohio State University, Columbus, OH 43210 3: ‡Laboratory of Comparative Carcinogenesis, National Cancer Institute-FCRDC, Frederick, MD 21702 4: §Comprehensive Cancer Center, The Ohio State University, Columbus, OH 43210

Publication date: April 1, 2001

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  • Gene Expression, The Journal of Liver Research will publish articles in all aspects of hepatology. Hepatology, as a research discipline, has seen unprecedented growth especially in the cellular and molecular mechanisms of hepatic health and disease, which continues to have a major impact on understanding liver development, stem cells, carcinogenesis, tissue engineering, injury, repair, regeneration, immunology, metabolism, fibrosis, and transplantation. Continued research and improved understanding in these areas will have a meaningful impact on liver disease prevention, diagnosis, and treatment. The existing journal Gene Expression has expanded its focus to become Gene Expression, The Journal of Liver Research to meet this growing demand. In its revised and expanded scope, the journal will publish high-impact original articles, reviews, short but complete articles, and special articles (editorials, commentaries, opinions) on all aspects of hepatology, making it a unique and invaluable resource for readers interested in this field. The expanded team, led by an Editor-in-Chief who is uniquely qualified and a renowned expert, along with a dynamic and functional editorial board, is determined to make this a premier journal in the field of hepatology.
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