Parthenolide treatment activates stress signaling proteins in high-risk acute lymphoblastic leukemia cells with chromosomal translocation t(4;11)

Susan J. Zunino, David H. Storms, Jonathan M Ducore

Research output: Contribution to journalArticle

8 Scopus citations


Parthenolide, the principal bio-active component of the herb feverfew (Tanacetum parthenium), has shown antileukemic activity. We evaluated the cell cycle status and the phosphorylation/activation of proteins involved in signal transduction in t(4;11) and non-t(4;11) acute lymphoblastic leukemia (ALL) cell lines after treatment with parthenolide. The cells were treated with the vehicle or 10 μM parthenolide for 2, 4, 6 and 8 h. As shown by flow cytometric analysis, parthenolide induced growth arrest at the S to G2/M phase transition. Using multiplex technology and Western blotting, we showed that the treatment with parthenolide within 0 to 10 h induced the phosphorylation of stress signaling proteins, including the p38 mitogen-activated protein kinase, the c-Jun N-terminal kinase, c-Jun, the heat shock protein 27 and protein kinase B. These data show that parthenolide induces a stress response leading to cell death and provide further evidence suggesting that parthenolide could be useful as a novel therapeutic agent against high risk ALL with chromosomal translocation t(4;11).

Original languageEnglish (US)
Pages (from-to)1307-1313
Number of pages7
JournalInternational Journal of Oncology
Issue number5
StatePublished - Nov 2010



  • Acute lymphoblastic leukemia
  • Parthenolide
  • Signal transduction
  • Stress response

ASJC Scopus subject areas

  • Cancer Research
  • Oncology

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