Evidence map›Paper›PMID 42737942›Full record

ArticleBiology2026

The Erk/CREB Signaling Axis Mediates G-CSF-Promoted G-MDSC Survival in the Peripheral Blood of Melanoma-Bearing Mice.

Yingying Sun, Yan Mo, Boya Xu, Chao Shang, Shu Jiang, Jing Xu, Yueshuang Ke, Xianlu Zeng

Abstract read
In one paragraph

Article in Biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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 SunSchool of Medicine, Huanghuai University, Zhumadian 463000, China.
Yan MoThe Key Laboratory of Molecular Epigenetics of Ministry of Education, Institute of Genetics and Cytology, School of Life Science, Northeast Normal University, Changchun 130024, China.ORCID 0000-0002-5419-6518
Boya XuThe Key Laboratory of Molecular Epigenetics of Ministry of Education, Institute of Genetics and Cytology, School of Life Science, Northeast Normal University, Changchun 130024, China.
Chao ShangThe Key Laboratory of Molecular Epigenetics of Ministry of Education, Institute of Genetics and Cytology, School of Life Science, Northeast Normal University, Changchun 130024, China.
Shu JiangThe Key Laboratory of Molecular Epigenetics of Ministry of Education, Institute of Genetics and Cytology, School of Life Science, Northeast Normal University, Changchun 130024, China.
Jing XuThe Key Laboratory of Molecular Epigenetics of Ministry of Education, Institute of Genetics and Cytology, School of Life Science, Northeast Normal University, Changchun 130024, China.ORCID 0009-0005-3325-8387
Yueshuang KeThe Key Laboratory of Molecular Epigenetics of Ministry of Education, Institute of Genetics and Cytology, School of Life Science, Northeast Normal University, Changchun 130024, China.ORCID 0000-0003-1518-4271
Xianlu ZengThe Key Laboratory of Molecular Epigenetics of Ministry of Education, Institute of Genetics and Cytology, School of Life Science, Northeast Normal University, Changchun 130024, China.ORCID 0000-0002-2655-4197

Funding

National Natural Science Foundation of China 31870888National Natural Science Foundation of China 32170916National Natural Science Foundation of China 81670095Youth Project of Henan Provincial Natural Science Foundation 262300420561
6 · The paper itself

Abstract

Myeloid-derived suppressor cells (MDSCs) are heterogeneous cell populations that promote tumor development by inhibiting innate and adaptive immunity. Under physiological conditions, neutrophils have a short survival time in vivo. However, G-MDSCs accumulate abnormally in most tumor hosts, and the mechanisms underlying G-MDSC persistence remain to be clarified. This study utilized flow cytometric analysis and in vivo assays to elucidate these mechanisms. It was observed that the apoptosis of G-MDSCs in the peripheral blood of mice was reduced under tumor conditions, whereas an increase in granulocyte colony-stimulating factor (G-CSF) promoted the survival of G-MDSCs. Furthermore, G-CSF reduced the apoptosis of G-MDSCs by activating the Erk/CREB pathway. Thus, inhibition of G-CSF/Erk/CREB signaling may promote the apoptosis of G-MDSCs and shorten their persistence under tumor conditions, as well as attenuate tumor progression.

Indexed as

Erk/CREB pathwayG-CSFG-MDSC persistencetumor conditions

Identifiers

PMID42737942
PMCPMC13564542

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.