Evidence map›Paper›PMID 40202509›Full record

ArticleThe Journal of experimental medicine2025

MYO1F in neutrophils is required for the response to immune checkpoint blockade therapy.

Yingying Qu, Wenhua Liang, Mingzhu Yu, Chenhui Wang, Min Luo, Lin Zhong, Zhigang Li, Feng Wang

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in The Journal of experimental medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

4 citing papers in PubMed.

  1. Review
  2. Article
  3. Review
  4. Review
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.

Yingying Qu *Institute of Pediatric Infection, Immunity, and Critical Care Medicine, Shanghai Children's Hospital, Shanghai Jiao Tong University School of Medicine , Shanghai, China.ORCID 0009-0003-5302-3759
Wenhua Liang *Institute of Pediatric Infection, Immunity, and Critical Care Medicine, Shanghai Children's Hospital, Shanghai Jiao Tong University School of Medicine , Shanghai, China.ORCID 0000-0002-8159-7720
Mingzhu YuInstitute of Pediatric Infection, Immunity, and Critical Care Medicine, Shanghai Children's Hospital, Shanghai Jiao Tong University School of Medicine , Shanghai, China.ORCID 0009-0009-1726-7194
Chenhui WangThe Key Laboratory for Human Disease Gene Study of Sichuan Province and the Department of Laboratory Medicine, Sichuan Provincial People's Hospital, University of Electronic Science and Technology of China, Chengdu, China.ORCID 0000-0002-3186-3066
Min LuoInstitute of Pediatrics of Children's Hospital of Fudan University, The Shanghai Key Laboratory of Medical Epigenetics, The International Co-laboratory of Medical Epigenetics and Metabolism, Ministry of Science and Technology, Institutes of Biomedical Sciences, Fudan University , Shanghai, China.ORCID 0000-0001-5732-4848
Lin ZhongDepartment of Liver Surgery and Organ Transplantation Center, Shenzhen Third People's Hospital, Second Affiliated Hospital, Southern University of Science and Technology, Shenzhen, China.ORCID 0000-0002-7811-9162
Zhigang LiDepartment of Thoracic Surgery, Shanghai Chest Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.ORCID 0000-0001-5086-5334
Feng WangInstitute of Pediatric Infection, Immunity, and Critical Care Medicine, Shanghai Children's Hospital, Shanghai Jiao Tong University School of Medicine , Shanghai, China.ORCID 0000-0002-3467-3700

Funding

Innovative Research Team of High-level Local University in ShanghaiNational Key Research and Development Program of China 2022YFA0912400National Natural Science Foundation of China 82230055Shanghai Jiao Tong UniversityState Key Laboratory of Medical GenomicsTechnology Committee of Shanghai Municipality 23DX1900302
6 · The paper itself

Abstract

Tumor-associated neutrophils (TANs) represent a significant barrier to the effectiveness of immune checkpoint blockade (ICB) therapy. A comprehensive understanding of TANs' regulatory mechanisms is therefore essential for predicting ICB efficacy and improving immunotherapy strategies. Our study reveals that MYO1F is selectively downregulated in neutrophils within both human cancers and murine tumor models, showing a negative correlation with ICB response. Mechanistically, MYO1F normally inhibits neutrophil immunosuppression and proliferation by restraining STAT3 activity. However, during tumorigenesis, tumor-derived TGF-β1 disrupts the binding of SPI1 to intron 8 of Myo1f via DNA methylation, thereby suppressing Myo1f transcription. The resultant decrease in MYO1F reprograms neutrophils into an immunosuppressive state through the STAT3-dependent signaling pathways. This immunosuppressive state further contributes to tumor microenvironment (TME) remodeling by inducing CTL exhaustion. These findings establish MYO1F as a critical regulator within TANs, highlighting its significant role in modulating ICB therapy efficacy.

Indexed as

Immune Checkpoint InhibitorsMyosin Type INeutrophilsAnimalsCell Line, TumorCell ProliferationDNA MethylationFemaleHumansImmunotherapyMiceMice, Inbred C57BLNeoplasmsSignal TransductionSTAT3 Transcription FactorTransforming Growth Factor beta1Immune Checkpoint InhibitorsMyosin Type ISTAT3 Transcription FactorTransforming Growth Factor beta1

Identifiers

PMID40202509
PMCPMC11980683

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.