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HMGA2 regulates transcription of the Imp2 gene via an intronic regulatory element in cooperation with nuclear factor-kappaB. | LitMetric

HMGA2 regulates transcription of the Imp2 gene via an intronic regulatory element in cooperation with nuclear factor-kappaB.

Mol Cancer Res

Department of Human Genetics, Flanders Interuniversity Institute for Biotechnology, University of Leuven, Herestraat 49, Box 602, B-3000 Leuven, Belgium.

Published: April 2007

AI Article Synopsis

  • IMP2 is an oncofetal protein involved in cancer, regulated by the transcription factor HMGA2 and its truncated form HMGA2Tr.
  • The study identified that HMGA2 binds to an AT-rich regulatory region in the Imp2 gene's first intron, influencing its transcription.
  • A significant correlation was found between HMGA2 and IMP2 expression levels in human liposarcomas, suggesting a cooperative role of HMGA2 and NF-kappaB in regulating Imp2 gene expression.

Article Abstract

IMP2 (insulin-like growth factor-II mRNA binding protein 2) is an oncofetal protein that is aberrantly expressed in several types of cancer. We recently identified the Imp2 gene as a target gene of the architectural transcription factor HMGA2 (high mobility group A2) and its tumor-specific truncated form HMGA2Tr. In this study, we investigated the mechanism via which HMGA2 regulates Imp2 gene expression. We show that HMGA2 and HMGA2Tr directly regulate transcription of the Imp2 gene by binding to an AT-rich regulatory region located in the first intron. In reporter experiments, we show that this AT-rich regulatory region mimics the response of the endogenous Imp2 gene to HMGA2 and HMGA2Tr. Furthermore, we show that a consensus nuclear factor-kappaB (NF-kappaB) binding site located immediately adjacent to the AT-rich regulatory region binds NF-kappaB and that NF-kappaB and HMGA2 cooperate to regulate Imp2 gene expression. Finally, we provide evidence that there is a strong and statistically significant correlation between HMGA2 and IMP2 gene expression in human liposarcomas.

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Source
http://dx.doi.org/10.1158/1541-7786.MCR-06-0331DOI Listing

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