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BioMed Research International
Volume 2015, Article ID 325026, 8 pages
http://dx.doi.org/10.1155/2015/325026
Research Article

Effects of a Particular Heptapeptide on the IFN-α-Sensitive CML Cells

1Department of Biochemistry, School of Life Sciences and The State Key Laboratory of Medical Genetics, Central South University, Changsha, Hunan 410013, China
2Department of Urology, The Second Xiangya Hospital of Central South University, Changsha, Hunan 410011, China
3Key Laboratory of Epigenetics and Oncology, The Research Center for Preclinical Medicine, Sichuan Medical University, Luzhou, Sichuan 646000, China
4Department of Biochemistry/Molecular Biology, Philadelphia College of Osteopathic Medicine, Philadelphia, PA 19131, USA

Received 24 June 2015; Revised 30 July 2015; Accepted 9 August 2015

Academic Editor: Massimo Breccia

Copyright © 2015 Fu-lan Yang 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

Using the phage display biopanning technique, we have previously identified a heptapeptide KLWVIPQ which specifically binds to the surface of the IFN-α-sensitive but not the IFN-α-resistant CML cells. The effects of this heptapeptide on the IFN-α-sensitive CML cells were investigated in the present study. IFN-α-sensitive KT-1/A3 and IFN-α-resistant KT-1/A3R CML cells were transfected by pEGFP-KLWVIPQ expression vector and/or induced by IFN-α. WST-1 cell proliferation assay, flow cytometry, and western blotting were performed to determine the effects of this heptapeptide and/or IFN-α on CML cells. The viability of the KT-1/A3 cells was inhibited and apoptosis was induced by either expression of the heptapeptide KLWVIPQ or IFN-α treatment with concurrent upregulation of P53 and downregulation of P210bcr/abl. However, these effects were not observed in the IFN-α-resistant KT-1/A3R cells. These results suggest that the heptapeptide KLWVIPQ shares a similar mechanism with IFN-α in the regulation of CML cell growth and apoptosis, implying that the heptapeptide KLWVIPQ could be a novel target to go further into mechanisms of IFN-α sensitivity and/or resistance in CML.