Sign in
Cancer BiologybioRxiv
Preprint

IL-32 is a metabolic regulator promoting survival and proliferation of malignant plasma cells

K. R. Aass, R. Mjelle, M. H. Kastnes, S. S. Tryggestad, L. M. van den Brink, M. Westhrin, M. Zahoor, S. H. Moen, G. Buene, K. Misund, A.-M. Sponaas, Q. Ma, A. Sundan, R. W. Groen, T. S. Slordahl, A. Waage, T. Standal

Abstract

IL-32 is a non-classical cytokine expressed in cancers, inflammatory diseases and infections. IL-32 can have both extracellular and intracellular functions, and its receptor is not identified. We here demonstrate that endogenously expressed, intracellular IL-32 binds to components of the mitochondrial respiratory chain and promotes oxidative phosphorylation. Knocking out IL-32 in malignant plasma cells significantly reduced survival and proliferation in vitro and in vivo. High throughput transcriptomic and MS-metabolomic profiling of IL-32 KO cells revealed that loss of IL-32 leads to profound perturbations in metabolic pathways, with accumulation of lipids, pyruvate precursors and citrate, indicative of reduced mitochondrial function. IL-32 is expressed in a subgroup of multiple myeloma patients with an inferior prognosis. Primary myeloma cells expressing IL-32 were characterized by a plasma cell gene signature associated with immune activation, proliferation and oxidative phosphorylation. We propose a novel concept for regulation of metabolism by an intracellular cytokine and identify IL-32 as an endogenous growth and survival factor for malignant plasma cells. IL-32 is a potential prognostic biomarker and a treatment target in multiple myeloma.

PDFDOI

02 /Specification & Classification

Click any tag to browse matching papers

Reproducibility ledger

Nobody has reported trying to reproduce this paper yet. Did you replicate an experiment or run the code? Your report saves the next lab a week.

Sign in to file a reproducibility report.