NDLI: Overexpression of human cyclin D1 reduces the transforming growth factor beta (TGF-beta) type II receptor and growth inhibition by TGF-beta 1 in an immortalized human esophageal epithelial cell line.

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Overexpression of human cyclin D1 reduces the transforming growth factor beta (TGF-beta) type II receptor and growth inhibition by TGF-beta 1 in an immortalized human esophageal epithelial cell line.

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Impact melting of frozen oceans on the early Earth: Implications for the origin of life

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Overexpression of human cyclin D1 reduces the transforming growth factor beta (TGF-beta) type II receptor and growth inhibition by TGF-beta 1 in an immortalized human esophageal epithelial cell line.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Spillare, E. A. Stoner, G. D. Jiang, W. Weinstein, I. B. Okamoto, A. Harris, C. C. Kim, S. J.
Description	Author Affiliation: Okamoto A ( Laboratory of Human Carcinogenesis, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892.);
Abstract	Cyclin D1 has been implicated in G1 cell cycle progression and is frequently amplified, overtranscribed, and oversynthesized in human tumors, including esophageal carcinomas. To further address the role of cyclin D1 in cell cycle control and tumorigenesis, we have stably transfected the human cyclin D1 in the nontumorigenic esophageal epithelial cell line HET-1A. These transfected cells, which express increased amounts of cyclin D1, have enhanced colony-forming efficiency and saturation density and are resistant to growth inhibition by TGF-beta 1 compared with the parental cell line or a control vector cell clone. The clones which express increased amounts of cyclin D1 exhibited a decrease in the amount of TGF-beta type II receptor, indicating a plausible mechanism for their diminished response to TGF-beta 1. Therefore, deregulated expression of the cyclin D1 gene can modulate the negative growth factor pathway of TGF-beta 1 and may disturb the control of epithelial cell proliferation in esophageal carcinogenesis.
ISSN	00278424
e-ISSN	10916490
Journal	Proceedings of the National Academy of Sciences of the United States of America
Issue Number	24
Volume Number	91
Language	English
Publisher	National Academy of Sciences
Publisher Date	1994-12-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Cyclin-Dependent Kinases Cyclins Metabolism Oncogene Proteins Proto-Oncogene Proteins Receptors, Transforming Growth Factor Beta Transforming Growth Factor Beta Pharmacology Cell Cycle Cell Line Cyclin D1 Cyclin-Dependent Kinase 4 Epithelial Cells Esophagus Cytology Gene Expression In Vitro Techniques Proliferating Cell Nuclear Antigen Protein-Serine-Threonine Kinases RNA, Messenger Genetics 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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