• Open Access

N-acetyl-cysteine enhances growth in BCR-ABL-transformed cells

Authors

  • QiGuo Zhang,

    1. Department of Pharmacology, Tokyo Women's Medical University, 8-1 Kawada-cho, Shinjuku-ku, Tokyo 162-8666, Japan
    Search for more papers by this author
  • Fujiko Tsukahara,

    1. Department of Pharmacology, Tokyo Women's Medical University, 8-1 Kawada-cho, Shinjuku-ku, Tokyo 162-8666, Japan
    Search for more papers by this author
  • Yoshiro Maru

    Corresponding author
    1. Department of Pharmacology, Tokyo Women's Medical University, 8-1 Kawada-cho, Shinjuku-ku, Tokyo 162-8666, Japan
      1To whom correspondence should be addressed. Email: ymaru@research.twmu.ac.jp
    Search for more papers by this author

1To whom correspondence should be addressed. Email: ymaru@research.twmu.ac.jp

Abstract

N-acetyl-cysteine (NAC) has been reported to have anticancer properties such as counteractions against mutagens and prevention of tumor progression by scavenging reactive oxygen species (ROS). However, here we report that NAC can enhance the anchorage-independent growth of cells transformed by activated ABL tyrosine kinases or Ras. This effect was not dependent on loss of focal adhesion kinase activation. NAC rescued cell growth that was suppressed by heat shock protein (Hsp) 90 inhibitors possibly by chemical modification of their quinone moiety. NAC rendered Rat1/BCR-ABL cells resistance to a Ras inhibitor manumycin in soft agar colony formation. In the absence of Hsp90 inhibitors, NAC stimulated the activation of MAP kinase in BCR-ABL-transformed but not in the parental Rat1 cells. We propose that NAC should be used carefully in cancer treatment. (Cancer Sci 2005; 96: 240 –244)

Ancillary