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. Proc Natl Acad Sci U S A 1994 Nov 22;91(24):11576-80
Date
11/22/1994Pubmed ID
7972105Pubmed Central ID
PMC45274DOI
10.1073/pnas.91.24.11576Scopus ID
2-s2.0-0027960437 (requires institutional sign-in at Scopus site) 87 CitationsAbstract
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.
Author List
Okamoto A, Jiang W, Kim SJ, Spillare EA, Stoner GD, Weinstein IB, Harris CCMESH terms used to index this publication - Major topics in bold
Cell CycleCell Line
Cyclin D1
Cyclin-Dependent Kinase 4
Cyclin-Dependent Kinases
Cyclins
Epithelial Cells
Esophagus
Gene Expression
Humans
In Vitro Techniques
Oncogene Proteins
Proliferating Cell Nuclear Antigen
Proto-Oncogene Proteins
RNA, Messenger
Receptors, Transforming Growth Factor beta
Transforming Growth Factor beta
