Evidence map›Paper›PMID 29968153›Full record

ArticleCancer immunology, immunotherapy : CII2018

mTOR-mediated glycolysis contributes to the enhanced suppressive function of murine tumor-infiltrating monocytic myeloid-derived suppressor cells.

Yuting Deng, Jiao Yang, Feifei Luo, Jing Qian, Ronghua Liu, Dan Zhang, Hongxiu Yu, Yiwei Chu

Open access · greenAbstract read
In one paragraph

Article in Cancer immunology, immunotherapy : CII, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

42 citing papers in PubMed, 53 citations in OpenAlex.

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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

8 authors at 2 institutions in 1 country.

Yuting DengDepartment of Immunology, School of Basic Medical Sciences, Fudan University, 138 Yi Xue Yuan Road, Shanghai, 200032, People's Republic of China.
Jiao YangDepartment of Immunology, School of Basic Medical Sciences, Fudan University, 138 Yi Xue Yuan Road, Shanghai, 200032, People's Republic of China.
Feifei LuoDepartment of Immunology, School of Basic Medical Sciences, Fudan University, 138 Yi Xue Yuan Road, Shanghai, 200032, People's Republic of China.
Jing QianDepartment of Immunology, School of Basic Medical Sciences, Fudan University, 138 Yi Xue Yuan Road, Shanghai, 200032, People's Republic of China.
Ronghua LiuDepartment of Immunology, School of Basic Medical Sciences, Fudan University, 138 Yi Xue Yuan Road, Shanghai, 200032, People's Republic of China.
Dan ZhangDepartment of Immunology, School of Basic Medical Sciences, Fudan University, 138 Yi Xue Yuan Road, Shanghai, 200032, People's Republic of China.
Hongxiu YuDepartment of Systems Biology for Medicine, School of Basic Medical Sciences and Institute of Biomedical Sciences, Fudan University, Shanghai, China.
Yiwei ChuDepartment of Immunology, School of Basic Medical Sciences, Fudan University, 138 Yi Xue Yuan Road, Shanghai, 200032, People's Republic of China. yiweichu@fudan.edu.cn.ORCID http://orcid.org/0000-0002-5035-1111
Fudan University · CNShanghai Medical College of Fudan University · CN

Funding

National Natural Science Foundation of China 31570892National Natural Science Foundation of China 81730045National Natural Science Foundation of China 91527305
6 · The paper itself

Abstract

Immune cell activation occurs concurrently with metabolic reprogramming. As important components of the tumor microenvironment, monocytic myeloid-derived suppressor cells (M-MDSCs) are featured by their potent immunosuppressive abilities on anti-tumor effector cells. However, little is known about the contribution of metabolic adaptations to their suppressive roles. In this study, we found that tumor-infiltrating M-MDSCs had the same phenotype with splenic M-MDSCs. Compared with splenic M-MDSCs, tumor-infiltrating M-MDSCs exhibited stronger suppressive activities which was accompanied by higher glycolysis. Inhibition of glycolysis impaired the suppressive function of tumor M-MDSCs. Meanwhile, the results demonstrated that mTOR was responsible for this function regulation. mTOR inhibition by rapamycin decreased the glycolysis and reduced the suppressive activities of these cells. Furthermore, rapamycin treatment inhibited the tumor growth and reduced the percentage of M-MDSCs in 3LL tumor bearing mice. These results demonstrated that modulation of metabolism in immune cells can be an effective way to enhance anti-tumor effects.

Indexed as

AnimalsAntibiotics, AntineoplasticCarcinoma, Lewis LungGlucoseGlycolysisMiceMice, Inbred C57BLMyeloid-Derived Suppressor CellsPhosphorylationSirolimusSpleenTOR Serine-Threonine KinasesAntibiotics, AntineoplasticGlucosemTOR protein, mouseSirolimusTOR Serine-Threonine KinasesGlycolysisImmunotherapyMDSCmTOR

Identifiers

PMID29968153
PMCPMC11028128
OpenAlexW2811142734

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.