ECop (EGFR-Coamplified and overexpressed protein), a novel protein, regulates NF-κB transcriptional activity and associated apoptotic response in an IκBα-dependent manner

S. Park, C. D. James*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

32 Scopus citations

Abstract

In the present study, we describe the function of a novel protein, ECop (EGFR-Coamplified and overexpressed protein), in the regulation of NF-κB activity. Ectopic expression of ECop increases NF-κB transcriptional activity by promoting nuclear translocation and DNA binding of NF-κB, and ECop-induced NF-κB activation confers cellular resistance to apoptotic challenge. In ECop knockdown cells, NF-κB transcriptional activity is suppressed due to delayed IκBα degradation, which results in a delayed nuclear translocation as well as decreased DNA binding of NF-κB. Suppression of NF-κB activation by ECop knockdown increases cellular susceptibility to apoptosis. These results suggest that ECop is a key regulator of NF-κB signaling, and that high-level, amplification-mediated ECop expression, such as that occurring in tumors with amplified EGFR, could contribute to resistance to apoptosis.

Original languageEnglish (US)
Pages (from-to)2495-2502
Number of pages8
JournalOncogene
Volume24
Issue number15
DOIs
StatePublished - Apr 7 2005

Keywords

  • Apoptosis
  • Ecop
  • Gene amplification
  • IκBα
  • NF-κB

ASJC Scopus subject areas

  • Molecular Biology
  • Genetics
  • Cancer Research

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