Targeting Mitochondria with Avocatin B Induces Selective Leukemia Cell Death

Cancer Res. 2015 Jun 15;75(12):2478-88. doi: 10.1158/0008-5472.CAN-14-2676.

Abstract

Treatment regimens for acute myeloid leukemia (AML) continue to offer weak clinical outcomes. Through a high-throughput cell-based screen, we identified avocatin B, a lipid derived from avocado fruit, as a novel compound with cytotoxic activity in AML. Avocatin B reduced human primary AML cell viability without effect on normal peripheral blood stem cells. Functional stem cell assays demonstrated selectivity toward AML progenitor and stem cells without effects on normal hematopoietic stem cells. Mechanistic investigations indicated that cytotoxicity relied on mitochondrial localization, as cells lacking functional mitochondria or CPT1, the enzyme that facilitates mitochondria lipid transport, were insensitive to avocatin B. Furthermore, avocatin B inhibited fatty acid oxidation and decreased NADPH levels, resulting in ROS-dependent leukemia cell death characterized by the release of mitochondrial proteins, apoptosis-inducing factor, and cytochrome c. This study reveals a novel strategy for selective leukemia cell eradication based on a specific difference in mitochondrial function.

MeSH terms

  • Animals
  • Apoptosis / drug effects
  • Cell Death / drug effects
  • Chromatography, Liquid / methods
  • Fruit / chemistry
  • High-Throughput Screening Assays / methods
  • Humans
  • Leukemia, Myeloid, Acute / drug therapy*
  • Leukemia, Myeloid, Acute / metabolism
  • Leukemia, Myeloid, Acute / pathology
  • Mass Spectrometry / methods
  • Mice
  • Mitochondria / drug effects*
  • Mitochondria / metabolism
  • Oxidation-Reduction
  • Persea / chemistry
  • Plant Extracts / pharmacology*
  • Plant Oils / pharmacology*
  • Reactive Oxygen Species / metabolism
  • Xenograft Model Antitumor Assays

Substances

  • Plant Extracts
  • Plant Oils
  • Reactive Oxygen Species