Evidence map›Paper›PMID 42498745›Full record

ArticleBritish journal of cancer2026

Lipid metabolic reprogramming of macrophage by host APOBEC3 deficiency enhances anti-tumor immunity.

Yuqi Yang, Fanglin Li, Mozi Lei, Yi Liu, Jiangling Lu, Chen Chen, Danyang Cui, Yiru Long, Xiaolu Yu, Jianhua Sun and 4 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in British journal of cancer, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0cells of the map it votes in
0citing papers in PubMed
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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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

14 authors.

Yuqi Yang *State Key Laboratory of Drug Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai, China.
Fanglin Li *State Key Laboratory of Drug Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai, China.ORCID http://orcid.org/0000-0003-2081-5437
Mozi LeiState Key Laboratory of Drug Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai, China.
Yi LiuSchool of Chinese Materia Medica, Nanjing University of Chinese Medicine, Nanjing, China.
Jiangling LuState Key Laboratory of Drug Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai, China.
Chen ChenState Key Laboratory of Drug Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai, China.
Danyang CuiState Key Laboratory of Drug Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai, China.
Yiru LongState Key Laboratory of Drug Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai, China.ORCID http://orcid.org/0000-0002-4525-4106
Xiaolu YuState Key Laboratory of Drug Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai, China.
Jianhua SunState Key Laboratory of Drug Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai, China.
Jing ChenState Key Laboratory of Drug Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai, China. jingchen@simm.ac.cn.ORCID http://orcid.org/0000-0003-3099-7238
Nan LiuState Key Laboratory of Drug Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai, China. Nan.Liu@PennMedicine.upenn.edu.ORCID http://orcid.org/0000-0002-6617-9897
Bingshun WangInstitute of Clinical Medicine, Ruijin Hospital LuWan Branch, Shanghai Jiao Tong University School of Medicine, Shanghai, China. wangbingshun@sjtu.edu.cn.ORCID http://orcid.org/0000-0002-0435-2543
Likun GongState Key Laboratory of Drug Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai, China. lkgong@simm.ac.cn.ORCID http://orcid.org/0000-0002-1896-4188

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundTumour-associated macrophages are an indispensable part of the tumour immune microenvironment, exhibiting phenotypic and functional plasticity that enables them to play an important role in modulating the immune response. A large number of RNA editing events have been identified during macrophage functional remodelling. APOBEC3 is a well-known family of base-editing enzymes, but whether and how it regulates macrophage function is unclear.

methodsIn this study, we mainly used genetically engineered mice to demonstrate how host APOBEC3 deficiency affects tumour progression.

resultsWe found that the polarisation state of macrophages in the tumour microenvironment was altered by host APOBEC3 deficiency and that knockout of host APOBEC3 significantly inhibited tumour growth and metastasis in a macrophage-dependent manner. Moreover, APOBEC3 deficiency remodelled macrophage function, improved their polarisation state, and enhanced their phagocytic capacity. Mechanistically, APOBEC3 knockout attenuated lipid uptake by macrophages in a PPARγ pathway-dependent way, leading to an increase of M1/M2 ratio in macrophages.

conclusionsThese findings reveal that APOBEC3 deficiency drives lipid metabolism reprogramming in macrophages and remodels their functions, thereby inducing a strong anti-tumour immune response, providing a proof-of-concept and new insights for the development of the APOBEC3 family for novel tumour therapies. Host APOBEC3 deficiency regulates macrophage function through lipid metabolic remodelling, ultimately leading to tumour suppression (Created with BioRender.com).

Indexed as

Cytidine DeaminaseLipid MetabolismMacrophagesTumor-Associated MacrophagesAnimalsMetabolic ReprogrammingMiceMice, KnockoutPPAR gammaTumor MicroenvironmentApobec3 protein, mouseCytidine DeaminasePPAR gamma

Identifiers

PMID42498745
PMCPMC13642954

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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.