B-cell non-Hodgkin lymphoma: Selective vulnerability to PIKFYVE inhibition

Autophagy. 2017 Jun 3;13(6):1082-1083. doi: 10.1080/15548627.2017.1304871. Epub 2017 Mar 28.

Abstract

We identified the PIKFYVE inhibitor apilimod as a potent and selective cytotoxic agent against B-cell non-Hodgkin lymphoma (B-NHL). Our data robustly establish PIKFYVE as the target through which apilimod kills B-NHL cells and show that apilimod-induced death in B-NHL is mediated by broad disruption of lysosome homeostasis characterized by lysosomal swelling, TFEB nuclear translocation, impaired maturation of lysosomal enzymes and incomplete autophagosome clearance. Furthermore, through genome-wide CRISPR knockout screening, we identified specific lysosomal genes (TFEB, CLCN7, OSTM1 and SNX10) as critical determinants of apilimod-induced cytotoxicity. Together these data highlight disruption of lysosome homeostasis through PIKFYVE inhibition as a novel anticancer mechanism in B-NHL and potentially other cancers.

Keywords: CLCN7; PIKFYVE; TFEB; apilimod; autophagy; lymphoma.

MeSH terms

  • B-Lymphocytes / drug effects
  • B-Lymphocytes / enzymology
  • B-Lymphocytes / pathology*
  • Endosomes / metabolism
  • Humans
  • Lymphoma, Non-Hodgkin / drug therapy*
  • Lymphoma, Non-Hodgkin / enzymology
  • Lymphoma, Non-Hodgkin / pathology
  • Lysosomes / metabolism
  • Models, Biological
  • Phosphatidylinositol 3-Kinases / metabolism
  • Phosphoinositide-3 Kinase Inhibitors*
  • Protein Kinase Inhibitors / pharmacology
  • Protein Kinase Inhibitors / therapeutic use*

Substances

  • Phosphoinositide-3 Kinase Inhibitors
  • Protein Kinase Inhibitors