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BioMed Research International
Volume 2014 (2014), Article ID 182353, 9 pages
Research Article

Pegylated Gold Nanoparticles Induce Apoptosis in Human Chronic Myeloid Leukemia Cells

1Department of Medical Research, China Medical University Hospital, Taichung 404, Taiwan
2School of Chinese Medicine, China Medical University, Taichung 404, Taiwan
3Department of Gynecology and Obstetrics, Mackay Memorial Hospital, Taipei 104, Taiwan
4Department of Medical Research, Mackay Memorial Hospital, Taipei 104, Taiwan
5Department of Pathology, Mackay Memorial Hospital, Taipei 104, Taiwan
6Institute of Physics, Academia Sinica, 128 Academia Road, Section 2, Taipei 115, Taiwan
7Department of Radiation Oncology, Mackay Memorial Hospital, 92 Chung San North Road, Section 2, Taipei 104, Taiwan
8Institute of Traditional Medicine, National Yang-Ming University, Taipei 112, Taiwan

Received 29 November 2013; Revised 4 February 2014; Accepted 15 February 2014; Published 25 March 2014

Academic Editor: Fabio Sonvico

Copyright © 2014 Yu-Chuen Huang 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.


Gold nanoparticles (AuNPs) have several potential biological applications as well as excellent biocompatibility. AuNPs with surface modification using polyethylene glycol (PEG-AuNPs) can facilitate easy conjugation with various biological molecules of interest. To examine the anticancer bioactivity of PEG-AuNPs, we investigated their effect on human chronic myeloid leukemia K562 cells. The results indicated that PEG-AuNPs markedly inhibited the viability and impaired the cell membrane integrity of K562 cells. The particles caused morphological changes typical of cell death, and a marked increase in the sub-G1 population in DNA histogram, indicating apoptosis. In addition, PEG-AuNPs reduced the mitochondrial transmembrane potential, a hallmark of the involvement of intrinsic apoptotic pathway in K562 cells. Observation of ultrastructure under a transmission electron microscope revealed that the internalized PEG-AuNPs were distributed into cytoplasmic vacuoles and damaged mitochondria, and subsequently accumulated in areas surrounding the nuclear membrane. In conclusion, PEG-AuNPs may have the potential to inhibit growth and induce apoptosis in human chronic myeloid leukemia cells.