Evidence map›Paper›PMID 37364932›Full record

ArticleJournal for immunotherapy of cancer2023

G-MDSC-derived exosomes mediate the differentiation of M-MDSC into M2 macrophages promoting colitis-to-cancer transition.

Yungang Wang, Hongli Liu, Zhe Zhang, Dezhi Bian, Keke Shao, Shengjun Wang, Yanxia Ding

Open access · goldAbstract read
In one paragraph

Article in Journal for immunotherapy of cancer, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
6.7field-weighted citation impact, top 3% 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

34 citing papers in PubMed, 41 citations in OpenAlex.

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  4. mAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
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  11. Natural carrier systems in cancer vaccines and immunotherapy.Human vaccines & immunotherapeutics · 2025
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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

7 authors at 3 institutions in 1 country.

Yungang Wang *Department of Laboratory Medicine, Dermatology, and Endocrinology, The Yancheng Clinical College of Xuzhou Medical University, The First people's Hospital of Yancheng, Yangcheng, China wzidyx2010@163.com wyg1223@126.com sjwjs@ujs.edu.cn.ORCID 0000-0001-6350-1660
Hongli Liu *Department of Clinical Laboratory, Nantong Tumor Hospital, Tumor Hospital Affiliated to Nantong University, Nantong, China.
Zhe ZhangDepartment of Laboratory Medicine, Dermatology, and Endocrinology, The Yancheng Clinical College of Xuzhou Medical University, The First people's Hospital of Yancheng, Yangcheng, China.
Dezhi BianDepartment of Laboratory Medicine, Dermatology, and Endocrinology, The Yancheng Clinical College of Xuzhou Medical University, The First people's Hospital of Yancheng, Yangcheng, China.
Keke ShaoDepartment of Laboratory Medicine, Dermatology, and Endocrinology, The Yancheng Clinical College of Xuzhou Medical University, The First people's Hospital of Yancheng, Yangcheng, China.
Shengjun WangDepartment of Immunology, Jiangsu Key Laboratory of Laboratory Medicine, School of Medicine Jiangsu University, Zhenjiang, China wzidyx2010@163.com wyg1223@126.com sjwjs@ujs.edu.cn.
Yanxia DingDepartment of Laboratory Medicine, Dermatology, and Endocrinology, The Yancheng Clinical College of Xuzhou Medical University, The First people's Hospital of Yancheng, Yangcheng, China wzidyx2010@163.com wyg1223@126.com sjwjs@ujs.edu.cn.ORCID 0000-0001-6584-1183
Xuzhou Medical College · CNJiangsu University · CNNantong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundsIn inflammatory bowel disease microenvironment, transdifferentiation of myeloid-derived suppressor cells (MDSCs) and M2 macrophage accumulation are crucial for the transition of colitis-to-cancer. New insights into the cross-talk and the underling mechanism between MDSCs and M2 macrophage during colitis-to-cancer transition are opening new avenues for colitis-associated cancer (CAC) prevention and treatment.

methodsThe role and underlying mechanism that granulocytic MDSCs (G-MDSCs) or exosomes (Exo) regulates the differentiation of monocytic MDSCs (M-MDSCs) into M2 macrophages were investigated using immunofluorescence, FACS, IB analysis, etc

resultsG-MDSCs promote the differentiation of M-MDSC into M2 macrophages through exosomal miR-93-5 p which downregulating STAT3 activity in M-MDSC. IL-6 is responsible for miR-93-5 p enrichment in G-MDSC exosomes (GM-Exo). Mechanistically, chronic inflammation-driven IL-6 promote the synthesis of miR-93-5 p in G-MDSC via IL-6R/JAK/STAT3 pathway. Early use of IL-6 Abs enhances the effect of STAT3 inhibitor against CAC.

conclusionsIL-6-driven secretion of G-MDSC exosomal miR-93-5 p promotes the differentiation of M-MDSC into M2 macrophages and involves a STAT3 signaling mechanism that promote colitis-to-cancer transition. Combining STAT3 inhibitors with strategies that inhibit IL-6-mediated G-MDSC exosomal miR-93-5 p production is beneficial for the prevention and treatment of CAC.

Indexed as

ColitisExosomesMicroRNAsMyeloid-Derived Suppressor CellsNeoplasmsAnimalsCell DifferentiationInterleukin-6MacrophagesMiceTumor MicroenvironmentInterleukin-6MicroRNAsgastrointestinal neoplasmsimmunotherapyinflammationmacrophagesmyeloid-derived suppressor cells

Identifiers

PMID37364932
PMCPMC10410840
OpenAlexW4382139581

What OpenQuestion holds

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LicenceCC BY-NC
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.