Bruceine D induces apoptosis in human chronic myeloid leukemia K562 cells via mitochondrial pathway

Jian-Ye Zhang, Min-Ting Lin, Ho-Yi Tung, Si-Li Tang, Tao Yi, Ya-Zhou Zhang, Yi-Na Tang, Zhong-Zhen Zhao, Hu-Biao Chen*

*Corresponding author for this work

Research output: Contribution to journalJournal articlepeer-review

52 Citations (Scopus)
22 Downloads (Pure)


Chronic myeloid leukemia (CML), an acquired malignant myeloproliferative disorder of hematopoietic stem cells, is one of the three most common forms of leukemia. In this study, we investigated the effects of bruceine D, which have been isolated from Brucea javanica (L.) Merr. on human chronic myeloid leukemia K562 cells. MTT assay was used to evaluate cell growth inhibition. Flow cytometry was performed to analyze mitochondrial membrane potential (Δψm). Western blot was applied to detect expression of cytochrome c, caspases-9, -3, PARP and other proteins. Bruceine D exhibited potent cytotoxicity to K562 cells with IC50 of 6.37 ± 0.39 μM. It led to loss of Δψm, release of cytochrome c, activation of caspases-9, -3 and cleavage of PARP, which suggested that bruceine D induced apoptosis of K562 cells through mitochondrial pathway. In addition, bruceine D inhibited the phosphorylation of AKT and ERK. It's indicative that the potent anticancer activity of bruceine D be related to MAPK and PI3K pathways.

Original languageEnglish
Pages (from-to)819-826
Number of pages8
JournalAmerican Journal of Cancer Research
Issue number4
Publication statusPublished - Apr 2016

Scopus Subject Areas

  • Oncology
  • Cancer Research

User-Defined Keywords

  • AKT
  • Apoptosis
  • Bruceine D
  • ERK
  • Mitochondrial pathway
  • Phosphorylation


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