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

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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.