The small molecule calactin induces DNA damage and apoptosis in human leukemia cells

Eur J Cancer Prev. 2012 Sep;21(5):467-73. doi: 10.1097/CEJ.0b013e3283498e66.


We purified calactin from the roots of the Chinese herb Asclepias curassavica L. and analyzed its biologic effects in human leukemia cells. Our results showed that calactin treatment caused DNA damage and resulted in apoptosis. Increased phosphorylation levels of Chk2 and H2AX were observed and were reversed by the DNA damage inhibitor caffeine in calactin-treated cells. In addition, calactin treatment showed that a decrease in the expression of cell cycle regulatory proteins Cyclin B1, Cdk1, and Cdc25C was consistent with a G2/M phase arrest. Furthermore, calactin induced extracellular signal-regulated kinase (ERK) phosphorylation, activation of caspase-3, caspase-8, and caspase-9, and PARP cleavage. Pretreatment with the ERK inhibitor PD98059 significantly blocked the loss of viability in calactin-treated cells. It is indicated that calactin-induced apoptosis may occur through an ERK signaling pathway. Our data suggest that calactin is a potential anticancer compound.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Antineoplastic Agents / therapeutic use*
  • Apoptosis*
  • Asclepias*
  • Cell Line, Tumor
  • DNA Damage*
  • Glycosides / therapeutic use*
  • Humans
  • Leukemia / drug therapy*
  • Phytotherapy*
  • Plant Preparations / therapeutic use
  • Plant Roots


  • Antineoplastic Agents
  • Glycosides
  • Plant Preparations