The Chinese-German Journal of Clinical Oncology

, Volume 6, Issue 4, pp 383–388

Characterization of cancer stem-like cells in a novel STI571-resistant chronic myeloid leukemia cell line

  • Baijun Fang
  • Yongping Song
  • Yanli Zhang
  • Quande Lin
  • Xudong Wei
Article

DOI: 10.1007/s10330-007-0012-9

Cite this article as:
Fang, B., Song, Y., Zhang, Y. et al. Chinese German J Clin Oncol (2007) 6: 383. doi:10.1007/s10330-007-0012-9

Abstract

Objective

To characterize a novel chronic myeloid leukemia (CML) cell line and to further elucidate the mechanisms of resistance to STI571.

Methods

A novel K562 cell line (K562/VP16) was achieved after exposure of the K562 cells to VP16. A small subpopulation (K562/VP16 SP) that was capable of excluding Hoechst 33342 in the K562/VP16 cell line was isolated by flow cytometry sorting. The rest of the K562/VP16 cells were classified as non-SP K562/VP16. The mechanisms involved in K562/VP16 SP cells which became resistant to STI571 were studied.

Results

The levels of Bcr-Abl and Abl proteins were similar in the K562 cell line and in non-SP K562/VP16 and K562/VP16 SP cells. The multidrug-resistant gene 1 (MDR1) expression of the 170 kDa P-glycoprotein (P-gp) was detected in K562/VP16 non-SP and K562/VP16 SP cells but not in K562 cells. The expression levels of P-gp in the two K562/VP16 cell lines were similar. Compared with non-SP K562/VP16, the K562/VP16 SP cells were more resistant to STI571. This resistance could hardly be reversed by many multidrug resistance inhibitors. In addition, in vivo study showed that the K562/VP16 SP cells induced tumorigenesis in mice, while the K562/VP16 non-SP cells failed to do so.

Conclusion

A novel K562 cell line, K562/VP16, was generated. A small side population K562/VP16 SP cells, had high resistance to STI571 treatment and more tumorigenic than the K562 cells. It may represent the cancer stem cells of the K562/VP16 cell line.

Key words

K562 cancer stem cell side population multidrug resistance 

Copyright information

© Editorial Office of the Chinese-German Journal of Clinical Oncology 2007

Authors and Affiliations

  • Baijun Fang
    • 1
  • Yongping Song
    • 1
  • Yanli Zhang
    • 1
  • Quande Lin
    • 1
  • Xudong Wei
    • 1
  1. 1.Henan Tumor Hospital, Henan Institute of Haematology, Henan Medical SchoolHenan UniversityZhengzhouChina

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