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Overexpression of USF increases TGF-beta1 protein levels, but G1 phase arrest was not induced in FRTL-5 cells
Cited 7 time in
Web of Science
Cited 8 time in Scopus
- Authors
- Issue Date
- 2008-10-29
- Publisher
- Korean Academy of Medical Science
- Citation
- J Korean Med Sci. 2008 Oct;23(5):870-6.
- Keywords
- Animals ; Binding Sites ; Cell Cycle ; Cell Line ; G1 Phase ; Promoter Regions, Genetic ; Protein Biosynthesis ; Rats ; Thymidine/chemistry ; Transfection ; Transforming Growth Factor beta1/metabolism ; Upstream Stimulatory Factors/*metabolism ; Apoptosis ; Gene Expression Regulation
- Abstract
- Transforming growth factor-beta1 (TGF-beta1) is a potent inhibitor of cellular growth and proliferation by G1 phase arrest or apoptosis. We investigated the association of TGF-beta1 with the anti-proliferative effect of upstream stimulatory factor (USF) in Fischer rat thyroid cell line (FRTL-5) cells. [methyl-(3)H] thymidine uptake was measured after treatment of FRTL-5 cells with TGF-beta1 to identify its anti-proliferative effect. USF-1 and USF-2 proteins were in vitro translated, and an electrophoretic mobility shift assay was performed to identify the interaction between USF and the TGF-beta1 promoter. FRTL-5 cells were transfected with USF cDNA, and then the expression of TGF-beta1 was examined with Northern and Western blotting. The cell cycle-regulating proteins associated with TGF-beta1 were also measured. TGF-beta1 significantly inhibited [methyl-(3)H] thymidine uptake in FRTL-5 cells. Two specific binding sites for USF were found in the TGF-beta1 promoter: -1,846 approximately -1,841 (CACATG) and -621 approximately -616 (CATGTG). Overexpression of USF increased both the mRNA levels and protein levels of TGF-beta1. However, the expression of cyclin D1, CDK4, cyclin E, and CDK2, and the phosphorylation of retinoblastoma protein remained unchanged. Overexpression of USF in FRTL-5 cells increased the expression of TGF-beta10 through specific binding to TGF-beta1 promoter. However, the USF-induced expression of TGF-beta1 did not cause G1 arrest.
- ISSN
- 1011-8934 (Print)
- Language
- English
- URI
- http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=18955796
http://synapse.koreamed.org/Synapse/Data/PDFData/0063JKMS/jkms-23-870.pdf
https://hdl.handle.net/10371/46310
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