Evidence map›Paper›PMID 29968710›Full record

ArticleNature communications2018

Monoacylglycerol lipase regulates cannabinoid receptor 2-dependent macrophage activation and cancer progression.

Wei Xiang, Rongchen Shi, Xia Kang, Xuan Zhang, Peng Chen, Lili Zhang, Along Hou, Rui Wang, Yuanyin Zhao, Kun Zhao and 13 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 151 papers.

0numbers the graph read from it
0cells of the map it votes in
151citing papers in PubMed
17.3field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

151 citing papers in PubMed, 235 citations in OpenAlex.

  1. Review
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  3. The biological functions of monoacylglycerol lipase (MAGL) in cancer.Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2026
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91 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

23 authors at 2 institutions in 1 country.

Wei XiangDepartment of Biochemistry and Molecular Biology, Third Military Medical University, Chongqing, 400038, China.
Rongchen ShiDepartment of Biochemistry and Molecular Biology, Third Military Medical University, Chongqing, 400038, China.
Xia KangDepartment of Biochemistry and Molecular Biology, Third Military Medical University, Chongqing, 400038, China.
Xuan ZhangDepartment of Oncology, Southwest Hospital, Third Military Medical University, Chongqing, 400038, China.
Peng ChenDepartment of General Surgery, PLA 324 Hospital, Chongqing, 400020, China.
Lili ZhangDepartment of Biochemistry and Molecular Biology, Third Military Medical University, Chongqing, 400038, China.
Along HouDepartment of Biochemistry and Molecular Biology, Third Military Medical University, Chongqing, 400038, China.
Rui WangDepartment of Biochemistry and Molecular Biology, Third Military Medical University, Chongqing, 400038, China.
Yuanyin ZhaoDepartment of Biochemistry and Molecular Biology, Third Military Medical University, Chongqing, 400038, China.
Kun ZhaoDepartment of Biochemistry and Molecular Biology, Third Military Medical University, Chongqing, 400038, China.
Yingzhe LiuDepartment of Biochemistry and Molecular Biology, Third Military Medical University, Chongqing, 400038, China.
Yue MaDepartment of Biochemistry and Molecular Biology, Third Military Medical University, Chongqing, 400038, China.
Huan LuoDepartment of Biochemistry and Molecular Biology, Third Military Medical University, Chongqing, 400038, China.
Shenglan ShangDepartment of Biochemistry and Molecular Biology, Third Military Medical University, Chongqing, 400038, China.
Jinyu ZhangNational Engineering Research Center of Immunological Products, Third Military Medical University, Chongqing, 400038, China.
Fengtian HeDepartment of Biochemistry and Molecular Biology, Third Military Medical University, Chongqing, 400038, China.
Songtao YuDepartment of Oncology, Southwest Hospital, Third Military Medical University, Chongqing, 400038, China.
Lixia GanDepartment of Biochemistry and Molecular Biology, Third Military Medical University, Chongqing, 400038, China.
Chunmeng ShiInstitute of Combined Injury, State Key Laboratory of Trauma, Burns and Combined Injury, Third Military Medical University, Chongqing, 400038, China.
Yongsheng LiClinical Medicine Research Center & Institute of Cancer, Xinqiao Hospital, Third Military Medical University, Chongqing, 400037, China. yli@tmmu.edu.cn.ORCID http://orcid.org/0000-0003-2175-9449
Wei YangDepartment of Pathology, School of Basic Medical Sciences & Nanfang Hospital, Southern Medical University, Guangzhou, 510515, China. yangwei@sibcb.ac.cn.ORCID http://orcid.org/0000-0001-9438-7215
Houjie LiangDepartment of Oncology, Southwest Hospital, Third Military Medical University, Chongqing, 400038, China. lianghoujie@sina.com.
Hongming MiaoDepartment of Biochemistry and Molecular Biology, Third Military Medical University, Chongqing, 400038, China. hongmingmiao@sina.com.
Army Medical University · CNNanfang Hospital · CN

Funding

National Natural Science Foundation of China (National Science Foundation of China) 31770931National Natural Science Foundation of China (National Science Foundation of China) 81672693
6 · The paper itself

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.

Indexed as

AgedAnimalsCD8-Positive T-LymphocytesCell Line, TumorDisease ProgressionFemaleHumansLipid MetabolismMacrophagesMaleMiceMice, Inbred BALB CMice, Inbred C57BLMice, KnockoutMiddle AgedMonoacylglycerol LipasesCNR2 protein, humanCnr2 protein, mouseMGLL protein, humanMgll protein, mouseMonoacylglycerol LipasesReceptor, Cannabinoid, CB2TLR4 protein, humanToll-Like Receptor 4

Identifiers

PMID29968710
PMCPMC6030061
OpenAlexW2809921982

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.