CaMKII γ, a critical regulator of CML stem/progenitor cells, is a target of the natural product berbamine.

نویسندگان

  • Ying Gu
  • Ting Chen
  • Zhipeng Meng
  • Yichao Gan
  • Xiaohua Xu
  • Guiyu Lou
  • Hongzhi Li
  • Xiaoxian Gan
  • Hong Zhou
  • Jinfen Tang
  • Genbo Xu
  • Liansheng Huang
  • Xiaohong Zhang
  • Yongming Fang
  • Kai Wang
  • Shu Zheng
  • Wendong Huang
  • Rongzhen Xu
چکیده

Bcr-Abl tyrosine kinase inhibitors (TKIs) have been a remarkable success for the treatment of Ph(+) chronic myeloid leukemia (CML). However, a significant proportion of patients treated with TKIs develop resistance because of leukemia stem cells (LSCs) and T315I mutant Bcr-Abl. Here we describe the unknown activity of the natural product berbamine that efficiently eradicates LSCs and T315I mutant Bcr-Abl clones. Unexpectedly, we identify CaMKII γ as a specific and critical target of berbamine for its antileukemia activity. Berbamine specifically binds to the ATP-binding pocket of CaMKII γ, inhibits its phosphorylation and triggers apoptosis of leukemia cells. More importantly, CaMKII γ is highly activated in LSCs but not in normal hematopoietic stem cells and coactivates LSC-related β-catenin and Stat3 signaling networks. The identification of CaMKII γ as a specific target of berbamine and as a critical molecular switch regulating multiple LSC-related signaling pathways can explain the unique antileukemia activity of berbamine. These findings also suggest that berbamine may be the first ATP-competitive inhibitor of CaMKII γ, and potentially, can serve as a new type of molecular targeted agent through inhibition of the CaMKII γ activity for treatment of leukemia.

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عنوان ژورنال:
  • Blood

دوره 120 24  شماره 

صفحات  -

تاریخ انتشار 2012