Table of Contents
Journal of Amino Acids
Volume 2013, Article ID 251398, 13 pages
http://dx.doi.org/10.1155/2013/251398
Research Article

The Antitumor Peptide CIGB-552 Increases COMMD1 and Inhibits Growth of Human Lung Cancer Cells

1Department of Genomic, Center for Genetic Engineering and Biotechnology, Cubanacan, P.O. Box 6162, 10600 Havana, Cuba
2Pharmaceutical Department, Laboratory of Cancer Biology, Center for Genetic Engineering and Biotechnology, Cubanacan, P.O. Box 6162, 10600 Havana, Cuba
3Cell Biology Unit, Institute Pasteur of Montevideo, Mataojo 2020, 11400 Montevideo, Uruguay
4Synthetic Peptide Group, Physical Chemistry Department, Center for Genetic Engineering and Biotechnology, Cubanacan, P.O. Box 6162, 10600 Havana, Cuba
5Center of Studies for Research and Biological Evaluations, Pharmacy and Food Sciences College, University of Havana, 19250 Havana, Cuba

Received 18 October 2012; Revised 12 December 2012; Accepted 12 December 2012

Academic Editor: Michele Caraglia

Copyright © 2013 Julio R. Fernández Massó et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

We have demonstrated that the peptide L-2 designed from an alanine scanning of the Limulus-derived LALF32-51 region is a potential candidate for the anticancer therapy and its cell-penetrating capacity is an associated useful property. By the modification in the primary structure of L-2, a second-generation peptide (CIGB-552) was developed. However, the molecular mechanism underlying its cytotoxic activity remains partially unknown. In this study, it was shown that CIGB-552 increases the levels of COMMD1, a protein involved in copper homeostasis, sodium transport, and the NF-κB signaling pathway. We found that CIGB-552 induces ubiquitination of RelA and inhibits the antiapoptotic activity regulated by NF-κB, whereas the knockdown of COMMD1 blocks this effect. We also found that CIGB-552 decreases the antioxidant capacity and induces the peroxidation of proteins and lipids in the tumor cells. Altogether, this study provides new insights into the mechanism of action of the peptide CIGB-552, which could be relevant in the design of future anticancer therapies.