Proteomic Study to Survey the CIGB-552 Antitumor Effect

Figure 8

Proposed mechanism for NF-κB signaling inhibition mediated by the antitumor peptide CIGB-552. Different proteins, which regulate NF-κB pathway, were differentially modulated by CIGB-552 treatment (TAX1BP1, SKP1, PSMA2/A2, and PSMA7/A7). In addition, the CIGB-552 target profile includes proteins that regulate RelA function (ETHE1, SETD7, and MAPK signaling: MAP2K6, MAPK14). Such interactions ultimately could repress the transcription of NF-κB target genes. Altogether, by modulating the function of these proteins CIGB-552 could inhibit cell proliferation and induces apoptosis of tumor cells.