Evidence map›Paper›PMID 40161370›Full record

ArticleFrontiers in oncology2025

OSMR induces M2 polarization of glioblastoma associated macrophages through JAK/STAT3 signaling pathway.

Changcheng Xiao, Liming Tan, Xiaofei Liu, Min Zhou, Ping Chen, Zhao Wang, Bing Wang

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Frontiers in oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing 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

5 citing papers in PubMed.

  1. Review
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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.

Changcheng XiaoDepartment of Neurosurgery, The Second Affiliated Hospital, Hengyang Medical School, University of South China, Hengyang, Hunan, China.
Liming TanDepartment of Neurosurgery, The Second Affiliated Hospital, Hengyang Medical School, University of South China, Hengyang, Hunan, China.
Xiaofei LiuDepartment of Neurosurgery, The Second Affiliated Hospital, Hengyang Medical School, University of South China, Hengyang, Hunan, China.
Min ZhouDepartment of Neurosurgery, The Second Affiliated Hospital, Hengyang Medical School, University of South China, Hengyang, Hunan, China.
Ping ChenDepartment of Neurosurgery, The Second Affiliated Hospital, Hengyang Medical School, University of South China, Hengyang, Hunan, China.
Zhao WangDepartment of Neurosurgery, The Second Affiliated Hospital, Hengyang Medical School, University of South China, Hengyang, Hunan, China.
Bing WangDepartment of Neurosurgery, The Second Affiliated Hospital, Hengyang Medical School, University of South China, Hengyang, Hunan, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Introduction: Verify whether Onconstatin M receptor (OSMR) plays a regulatory role in the growth of glioblastoma (GBM) and explore its specific regulatory mechanism. Methods: Results: Knocking down OSMR dramatically reduces tumor cell proliferation, invasion, and migration, accelerates cell death and cell cycle arrest, and lowers JAK and STAT3 phosphorylation as well as CCL-2 expression levels, all while decreasing the fraction of M2 macrophages. Furthermore, knocking down OSMR drastically lowered tumor development and M2 polarization levels of monocytes in tumor tissue. JAKa reversed the inhibitory effect of OSMR knockdown on GBM malignant development and macrophage M2 polarization in both Conclusion: OSMR promotes the JAK/STAT3 signaling pathway, which promotes malignant glioblastoma growth and macrophages M2 polarization.

Indexed as

glioblastomaJAK/STAT3 signaling pathwayM2 polarizationmacrophageOSMR

Identifiers

PMID40161370
PMCPMC11949811

What OpenQuestion holds

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Registered trials

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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.