Identification of E2F1 as a positive transcriptional regulator for {delta}-catenin
- Department of Anatomy and Cell Biology, Brody School of Medicine, East Carolina University, 600 Moye Street, Greenville, NC 27834 (United States)
- College of Pharmacy and Research Institute of Drug development, Chonnam National University, Gwangju 500-757 (Korea, Republic of)
- Bascom Palmer Eye Institute, Miller School of Medicine, University of Miami, Miami, FL 33136 (United States)
- Department of Pathology, Harvard Medical School, Boston, MA 20115 (United States)
{delta}-Catenin is upregulated in human carcinomas. However, little is known about the potential transcriptional factors that regulate {delta}-catenin expression in cancer. Using a human {delta}-catenin reporter system, we have screened several nuclear signaling modulators to test whether they can affect {delta}-catenin transcription. Among {beta}-catenin/LEF-1, Notch1, and E2F1, E2F1 dramatically increased {delta}-catenin-luciferase activities while {beta}-catenin/LEF-1 induced only a marginal increase. Rb suppressed the upregulation of {delta}-catenin-luciferase activities induced by E2F1 but did not interact with {delta}-catenin. RT-PCR and Western blot analyses in 4 different prostate cancer cell lines revealed that regulation of {delta}-catenin expression is controlled mainly at the transcriptional level. Interestingly, the effects of E2F1 on {delta}-catenin expression were observed only in human cancer cells expressing abundant endogenous {delta}-catenin. These studies identify E2F1 as a positive transcriptional regulator for {delta}-catenin, but further suggest the presence of strong negative regulator(s) for {delta}-catenin in prostate cancer cells with minimal endogenous {delta}-catenin expression.
- OSTI ID:
- 21143643
- Journal Information:
- Biochemical and Biophysical Research Communications, Vol. 369, Issue 2; Other Information: DOI: 10.1016/j.bbrc.2008.02.069; PII: S0006-291X(08)00290-8; Copyright (c) 2008 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved; Country of input: International Atomic Energy Agency (IAEA); ISSN 0006-291X
- Country of Publication:
- United States
- Language:
- English
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