Pharmacological inhibition of LSD1 for the treatment of MLL-rearranged leukemia

J Hematol Oncol. 2016 Mar 12:9:24. doi: 10.1186/s13045-016-0252-7.

Abstract

Background: Mixed lineage leukemia (MLL) gene translocations are found in ~75% infant and 10% adult acute leukemia, showing a poor prognosis. Lysine-specific demethylase 1 (LSD1) has recently been implicated to be a drug target for this subtype of leukemia. More studies using potent LSD1 inhibitors against MLL-rearranged leukemia are needed.

Methods: LSD1 inhibitors were examined for their biochemical and biological activities against LSD1 and MLL-rearranged leukemia as well as other cancer cells.

Results: Potent LSD1 inhibitors with biochemical IC50 values of 9.8-77 nM were found to strongly inhibit proliferation of MLL-rearranged leukemia cells with EC50 of 10-320 nM, while these compounds are generally non-cytotoxic to several other tumor cells. LSD1 inhibition increased histone H3 lysine 4 (H3K4) methylation, downregulated expression of several leukemia-relevant genes, induced apoptosis and differentiation, and inhibited self-renewal of stem-like leukemia cells. Moreover, LSD1 inhibitors worked synergistically with inhibition of DOT1L, a histone H3 lysine 79 (H3K79) methyltransferase, against MLL-rearranged leukemia. The most potent LSD1 inhibitor showed significant in vivo activity in a systemic mouse model of MLL-rearranged leukemia without overt toxicities. Mechanistically, LSD1 inhibitors caused significant upregulation of several pathways that promote hematopoietic differentiation and apoptosis.

Conclusions: LSD1 is a drug target for MLL-rearranged leukemia, and LSD1 inhibitors are potential therapeutics for the malignancy.

Keywords: Drug discovery; Enzyme inhibitor; Leukemia therapeutics; Lysine-specific demethylase 1; MLL-rearranged leukemia.

Publication types

  • Research Support, N.I.H., Extramural

MeSH terms

  • Animals
  • Blotting, Western
  • Cell Line, Tumor
  • Cell Proliferation / drug effects
  • Cell Proliferation / genetics
  • Child
  • Drug Synergism
  • Enzyme Inhibitors / chemistry
  • Enzyme Inhibitors / pharmacology*
  • Gene Expression Regulation, Leukemic / drug effects
  • Gene Rearrangement*
  • Histone Demethylases / antagonists & inhibitors*
  • Histone Demethylases / genetics
  • Histone Demethylases / metabolism
  • Histone-Lysine N-Methyltransferase / genetics*
  • Histones / metabolism
  • Humans
  • Leukemia / drug therapy*
  • Leukemia / genetics
  • Leukemia / metabolism
  • Lysine / metabolism
  • MCF-7 Cells
  • Methylation / drug effects
  • Methyltransferases / antagonists & inhibitors
  • Methyltransferases / genetics
  • Methyltransferases / metabolism
  • Mice, Inbred NOD
  • Mice, SCID
  • Molecular Structure
  • Monoamine Oxidase Inhibitors / chemistry
  • Monoamine Oxidase Inhibitors / pharmacology
  • Myeloid-Lymphoid Leukemia Protein / genetics*
  • Reverse Transcriptase Polymerase Chain Reaction
  • U937 Cells
  • Xenograft Model Antitumor Assays

Substances

  • Enzyme Inhibitors
  • Histones
  • KMT2A protein, human
  • Monoamine Oxidase Inhibitors
  • Myeloid-Lymphoid Leukemia Protein
  • Histone Demethylases
  • KDM1A protein, human
  • DOT1L protein, human
  • Methyltransferases
  • Histone-Lysine N-Methyltransferase
  • Lysine