Evidence map›Paper›PMID 28092673›Full record

ArticleOncogene2017

IRF7 regulates the development of granulocytic myeloid-derived suppressor cells through S100A9 transrepression in cancer.

Q Yang, X Li, H Chen, Y Cao, Q Xiao, Y He, J Wei, J Zhou

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

37 citing papers in PubMed, 56 citations in OpenAlex.

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  7. Neuropilin-1Cellular & molecular immunology · 2024
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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 4 institutions in 1 country.

Q YangProgram in Immunology, Affiliated Guangzhou Women and Children's Medical Center, Zhongshan School of Medicine, Guangzhou, China.
X LiInstitute of Human Virology, Zhongshan School of Medicine, Sun Yat-Sen University, Guangzhou, China.
H ChenInstitute of Human Virology, Zhongshan School of Medicine, Sun Yat-Sen University, Guangzhou, China.
Y CaoInstitute of Human Virology, Zhongshan School of Medicine, Sun Yat-Sen University, Guangzhou, China.
Q XiaoInstitute of Human Virology, Zhongshan School of Medicine, Sun Yat-Sen University, Guangzhou, China.
Y HeInstitute of Human Virology, Zhongshan School of Medicine, Sun Yat-Sen University, Guangzhou, China.
J WeiInstitute of Human Virology, Zhongshan School of Medicine, Sun Yat-Sen University, Guangzhou, China.
J ZhouProgram in Immunology, Affiliated Guangzhou Women and Children's Medical Center, Zhongshan School of Medicine, Guangzhou, China.
Sun Yat-sen University · CNGuangzhou Medical University · CNGuangzhou Women and Children Medical Center · CNThird Affiliated Hospital of Sun Yat-sen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Accumulation of myeloid-derived suppressor cells (MDSCs) is one of the major obstacles against achieving appropriate anti-tumor immune responses and successful tumor immunotherapy. Granulocytic MDSCs (G-MDSCs) are common in tumor-bearing hosts. However, the mechanisms regulating the development of MDSCs, especially G-MDSCs, remain poorly understood. In this report, we showed that interferon regulatory factor 7 (IRF7) plays an important role in the development of G-MDSCs, but not monocytic MDSCs. IRF7 deficiency caused significant elevation of G-MDSCs, and therefore enhanced tumor growth and metastasis in mice. IRF7 deletion did not affect the suppressive activity of G-MDSCs. Mechanistic studies showed that S100A9, a negative regulator of myeloid cell differentiation, was transrepressed by the IRF7 protein. S100A9 knockdown almost completely abrogated the effects of IRF7 deletion on G-MDSC development and tumor metastasis. Importantly, IRF7 expression levels negatively correlated with the G-MDSC frequency and tumor metastasis, as well as S100A9 expression, in cancer patients. In summary, our study demonstrated that IRF7 represents a novel regulator of G-MDSC development in cancer, which may have predictive value for tumor progression.

Indexed as

AnimalsBiomarkers, TumorCalgranulin BCell DifferentiationCell Line, TumorDown-RegulationGene Expression Regulation, NeoplasticGranulocytesHumansImmunotherapyInterferon Regulatory Factor-7MiceMice, Inbred C57BLMice, KnockoutMyeloid-Derived Suppressor CellsNeoplasmsBiomarkers, TumorCalgranulin BInterferon Regulatory Factor-7

Identifiers

PMID28092673
OpenAlexW2573760796

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.