A role for macrophages under cytokine control in mediating resistance to ADI-PEG20 (pegargiminase) in ASS1-deficient mesothelioma

Pharmacol Rep. 2023 Jun;75(3):570-584. doi: 10.1007/s43440-023-00480-6. Epub 2023 Apr 3.

Abstract

Background: Pegylated arginine deiminase (ADI-PEG20; pegargiminase) depletes arginine and improves survival outcomes for patients with argininosuccinate synthetase 1 (ASS1)-deficient malignant pleural mesothelioma (MPM). Optimisation of ADI-PEG20-based therapy will require a deeper understanding of resistance mechanisms, including those mediated by the tumor microenvironment. Here, we sought to reverse translate increased tumoral macrophage infiltration in patients with ASS1-deficient MPM relapsing on pegargiminase therapy.

Methods: Macrophage-MPM tumor cell line (2591, MSTO, JU77) co-cultures treated with ADI-PEG20 were analyzed by flow cytometry. Microarray experiments of gene expression profiling were performed in ADI-PEG20-treated MPM tumor cells, and macrophage-relevant genetic "hits" were validated by qPCR, ELISA, and LC/MS. Cytokine and argininosuccinate analyses were performed using plasma from pegargiminase-treated patients with MPM.

Results: We identified that ASS1-expressing macrophages promoted viability of ADI-PEG20-treated ASS1-negative MPM cell lines. Microarray gene expression data revealed a dominant CXCR2-dependent chemotactic signature and co-expression of VEGF-A and IL-1α in ADI-PEG20-treated MPM cell lines. We confirmed that ASS1 in macrophages was IL-1α-inducible and that the argininosuccinate concentration doubled in the cell supernatant sufficient to restore MPM cell viability under co-culture conditions with ADI-PEG20. For further validation, we detected elevated plasma VEGF-A and CXCR2-dependent cytokines, and increased argininosuccinate in patients with MPM progressing on ADI-PEG20. Finally, liposomal clodronate depleted ADI-PEG20-driven macrophage infiltration and suppressed growth significantly in the MSTO xenograft murine model.

Conclusions: Collectively, our data indicate that ADI-PEG20-inducible cytokines orchestrate argininosuccinate fuelling of ASS1-deficient mesothelioma by macrophages. This novel stromal-mediated resistance pathway may be leveraged to optimize arginine deprivation therapy for mesothelioma and related arginine-dependent cancers.

Keywords: ADI-PEG20; ASS1; Arginine deprivation; Macrophages; Mesothelioma.

MeSH terms

  • Animals
  • Arginine / metabolism
  • Argininosuccinate Synthase / genetics
  • Argininosuccinate Synthase / metabolism
  • Cell Line, Tumor
  • Drug Resistance, Neoplasm*
  • Humans
  • Macrophages*
  • Mesothelioma* / drug therapy
  • Mesothelioma* / genetics
  • Mesothelioma, Malignant*
  • Mice
  • Neoplasm Recurrence, Local
  • Polyethylene Glycols / pharmacology
  • Tumor Microenvironment
  • Vascular Endothelial Growth Factor A

Substances

  • ADI PEG20
  • Arginine
  • Argininosuccinate Synthase
  • Polyethylene Glycols
  • Vascular Endothelial Growth Factor A