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Targeting FROUNT with disulfiram suppresses macrophage accumulation and its tumor-promoting properties.

Abstract：

:Tumor-associated macrophages affect tumor progression and resistance to immune checkpoint therapy. Here, we identify the chemokine signal regulator FROUNT as a target to control tumor-associated macrophages. The low level FROUNT expression in patients with cancer correlates with better clinical outcomes. Frount-deficiency markedly reduces tumor progression and decreases macrophage tumor-promoting activity. FROUNT is highly expressed in macrophages, and its myeloid-specific deletion impairs tumor growth. Further, the anti-alcoholism drug disulfiram (DSF) acts as a potent inhibitor of FROUNT. DSF interferes with FROUNT-chemokine receptor interactions via direct binding to a specific site of the chemokine receptor-binding domain of FROUNT, leading to inhibition of macrophage responses. DSF monotherapy reduces tumor progression and decreases macrophage tumor-promoting activity, as seen in the case of Frount-deficiency. Moreover, co-treatment with DSF and an immune checkpoint antibody synergistically inhibits tumor growth. Thus, inhibition of FROUNT by DSF represents a promising strategy for macrophage-targeted cancer therapy.

journal_name

Nat Commun

journal_title

Nature communications

authors

Terashima Y,Toda E,Itakura M,Otsuji M,Yoshinaga S,Okumura K,Shand FHW,Komohara Y,Takeda M,Kokubo K,Chen MC,Yokoi S,Rokutan H,Kofuku Y,Ohnishi K,Ohira M,Iizasa T,Nakano H,Okabe T,Kojima H,Shimizu A,Kanegasaki S,

doi

10.1038/s41467-020-14338-5

subject

Has Abstract

pub_date

2020-01-30 00:00:00

pages

609

issue

1

issn

2041-1723

pii

10.1038/s41467-020-14338-5

journal_volume

11

pub_type

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