Identification of E2F1 as a positive transcriptional regulator for delta-catenin.

Abstract

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.

• Authors: Kwonseop Kim, Minsoo Oh, Hyunkyoung Ki, Tao Wang, Sonja Bareiss, M Elizabeth Fini, Dawei Li, Qun Lu
• Journal: Biochemical and biophysical research communications (Biochem Biophys Res Commun) Vol. 369 Issue 2 Pg. 414-20 (May 02 2008) ISSN: 1090-2104 [Electronic] United States
• PMID: 18302937 (Publication Type: Journal Article, Research Support, N.I.H., Extramural, Research Support, Non-U.S. Gov't, Research Support, U.S. Gov't, Non-P.H.S.)

Chemical References

• Catenins
• Cell Adhesion Molecules
• E2F1 Transcription Factor
• E2F1 protein, human
• Phosphoproteins
• Delta Catenin

Topics

• Catenins
• Cell Adhesion Molecules (metabolism)
• Cell Line, Tumor
• E2F1 Transcription Factor (genetics, metabolism)
• Gene Expression Regulation, Neoplastic
• Humans
• Male
• Phosphoproteins (metabolism)
• Prostatic Neoplasms (genetics, metabolism)
• Signal Transduction
• Transcriptional Activation
• Delta Catenin