Abstract:
:Metabolic reprogramming greatly contributes to the regulation of macrophage activation. However, the mechanism of lipid accumulation and the corresponding function in tumor-associated macrophages (TAMs) remain unclear. With primary investigation in colon cancer and confirmation in other cancer models, here we determine that deficiency of monoacylglycerol lipase (MGLL) results in lipid overload in TAMs. Functionally, macrophage MGLL inhibits CB2 cannabinoid receptor-dependent tumor progression in inoculated and genetic cancer models. Mechanistically, MGLL deficiency promotes CB2/TLR4-dependent macrophage activation, which further suppresses the function of tumor-associated CD8+ T cells. Treatment with CB2 antagonists delays tumor progression in inoculated and genetic cancer models. Finally, we verify that expression of macrophage MGLL is decreased in cancer tissues and positively correlated with the survival of cancer patients. Taken together, our findings identify MGLL as a switch for CB2/TLR4-dependent macrophage activation and provide potential targets for cancer therapy.
journal_name
Nat Communjournal_title
Nature communicationsauthors
Xiang W,Shi R,Kang X,Zhang X,Chen P,Zhang L,Hou A,Wang R,Zhao Y,Zhao K,Liu Y,Ma Y,Luo H,Shang S,Zhang J,He F,Yu S,Gan L,Shi C,Li Y,Yang W,Liang H,Miao Hdoi
10.1038/s41467-018-04999-8subject
Has Abstractpub_date
2018-07-03 00:00:00pages
2574issue
1issn
2041-1723pii
10.1038/s41467-018-04999-8journal_volume
9pub_type
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