α-Tomatine-mediated anti-cancer activity in vitro and in vivo through cell cycle- and caspase-independent pathways

PLoS One. 2012;7(9):e44093. doi: 10.1371/journal.pone.0044093. Epub 2012 Sep 6.

Abstract

α-Tomatine, a tomato glycoalkaloid, has been reported to possess antibiotic properties against human pathogens. However, the mechanism of its action against leukemia remains unclear. In this study, the therapeutic potential of α-tomatine against leukemic cells was evaluated in vitro and in vivo. Cell viability experiments showed that α-tomatine had significant cytotoxic effects on the human leukemia cancer cell lines HL60 and K562, and the cells were found to be in the Annexin V-positive/propidium iodide-negative phase of cell death. In addition, α-tomatine induced both HL60 and K562 cell apoptosis in a cell cycle- and caspase-independent manner. α-Tomatine exposure led to a loss of the mitochrondrial membrane potential, and this finding was consistent with that observed on activation of the Bak and Mcl-1 short form (Mcl-1s) proteins. Exposure to α-tomatine also triggered the release of the apoptosis-inducing factor (AIF) from the mitochondria into the nucleus and down-regulated survivin expression. Furthermore, α-tomatine significantly inhibited HL60 xenograft tumor growth without causing loss of body weight in severe combined immunodeficiency (SCID) mice. Immunohistochemical test showed that the reduced tumor growth in the α-tomatine-treated mice was a result of increased apoptosis, which was associated with increased translocation of AIF in the nucleus and decreased survivin expression ex vivo. These results suggest that α-tomatine may be a candidate for leukemia treatment.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Antineoplastic Agents / chemistry
  • Antineoplastic Agents / pharmacology*
  • Apoptosis / drug effects
  • Apoptosis Inducing Factor / metabolism
  • Caspases / metabolism
  • Cell Cycle / drug effects*
  • Cell Nucleus / drug effects
  • Cell Nucleus / metabolism
  • Down-Regulation / drug effects
  • Enzyme Activation / drug effects
  • HL-60 Cells
  • Humans
  • Inhibitor of Apoptosis Proteins / metabolism
  • K562 Cells
  • Membrane Potential, Mitochondrial / drug effects
  • Mice
  • Mice, SCID
  • Neoplasm Proteins / metabolism
  • Protein Transport / drug effects
  • Signal Transduction / drug effects*
  • Survivin
  • Tomatine / analogs & derivatives*
  • Tomatine / chemistry
  • Tomatine / pharmacology
  • Xenograft Model Antitumor Assays

Substances

  • Antineoplastic Agents
  • Apoptosis Inducing Factor
  • BIRC5 protein, human
  • Inhibitor of Apoptosis Proteins
  • Neoplasm Proteins
  • Survivin
  • alpha-tomatine
  • Tomatine
  • Caspases

Grants and funding

This study was supported by Grants from the National Science Council of Taiwan (NSC 99-2320-B400-008-MY3) and (NSC 99-2628-B002-024-MY3). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.