Evidence map›Paper›PMID 30171602›Full record

ArticleImmunology2019

Deceleration of glycometabolism impedes IgG-producing B-cell-mediated tumor elimination by targeting SATB1.

Jiajing Liu, Yifan Li, Zhou Lu, Jie Gu, Yun Liang, Enyu Huang, Zhiming Wang, Hushan Zhang, Luman Wang, Dan Zhang and 3 more

Abstract read
In one paragraph

Article in Immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
–field-weighted citation impact
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

18 citing papers in PubMed.

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  13. Journal of thoracic disease · 2023
    Article
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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

13 authors.

Jiajing LiuDepartment of Immunology, School of Basic Medical Sciences, Institute of Biomedical Sciences, Fudan University, Shanghai, China.
Yifan LiDepartment of Immunology, School of Basic Medical Sciences, Institute of Biomedical Sciences, Fudan University, Shanghai, China.
Zhou LuDepartment of Immunology, School of Basic Medical Sciences, Institute of Biomedical Sciences, Fudan University, Shanghai, China.
Jie GuDepartment of Thoracic Surgery, The Affiliated Zhongshan Hospital of Fudan University, Shanghai, China.
Yun LiangDepartment of Orthopedics, The Affiliated Zhongshan Hospital of Fudan University, Shanghai, China.
Enyu HuangDepartment of Immunology, School of Basic Medical Sciences, Institute of Biomedical Sciences, Fudan University, Shanghai, China.
Zhiming WangDepartment of Immunology, School of Basic Medical Sciences, Institute of Biomedical Sciences, Fudan University, Shanghai, China.
Hushan ZhangDepartment of Immunology, School of Basic Medical Sciences, Institute of Biomedical Sciences, Fudan University, Shanghai, China.
Luman WangDepartment of Immunology, School of Basic Medical Sciences, Institute of Biomedical Sciences, Fudan University, Shanghai, China.
Dan ZhangDepartment of Immunology, School of Basic Medical Sciences, Institute of Biomedical Sciences, Fudan University, Shanghai, China.
Hongxiu YuInstitute of Biomedical Sciences, Fudan University, Shanghai, China.
Ronghua LiuDepartment of Immunology, School of Basic Medical Sciences, Institute of Biomedical Sciences, Fudan University, Shanghai, China.
Yiwei ChuDepartment of Immunology, School of Basic Medical Sciences, Institute of Biomedical Sciences, Fudan University, Shanghai, China.ORCID 0000-0002-5035-1111

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

B lymphocytes, known as antibody producers, mediate tumor cell destruction in the manner of antibody-dependent cell-mediated cytotoxicity; however, their anti-tumor function seems to be weakened during tumorigenesis, while the underlying mechanisms remain unclear. In this study, we found that IgG mediated anti-tumor effects, but IgG-producing B cells decreased in various tumors. Considering the underlying mechanism, glycometabolism was noteworthy. We found that tumor-infiltrating B cells were glucose-starved and accompanied by a deceleration of glycometabolism. Both inhibition of glycometabolism and deprivation of glucose through tumor cells, or glucose-free treatment, reduced the differentiation of B cells into IgG-producing cells. In this process, special AT-rich sequence-binding protein-1 (SATB1) was significantly silenced in B cells. Down-regulating SATB1 by inhibiting glycometabolism or RNA interference reduced the binding of signal transducer and activator of transcription 6 (STAT6) to the promoter of germline Cγ gene, subsequently resulting in fewer B cells producing IgG. Our findings provide the first evidence that glycometabolic inhibition by tumorigenesis suppresses differentiation of B cells into IgG-producing cells, and altering glycometabolism may be promising in improving the anti-tumor effect of B cells.

Indexed as

AdenocarcinomaAgedAnimalsAzoxymethaneB-LymphocytesCells, CulturedColorectal NeoplasmsDextran SulfateDisease Models, AnimalFemaleGlucoseHumansImmunoglobulin GLung NeoplasmsMaleMatrix Attachment Region Binding ProteinsAzoxymethaneDextran SulfateGlucoseImmunoglobulin GMatrix Attachment Region Binding ProteinsRNA, Small InterferingSatb1 protein, mouseSTAT6 Transcription FactorB cellsmetabolic disordertumor immunology

Identifiers

PMID30171602
PMCPMC6283656

What OpenQuestion holds

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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.