Evidence map›Paper›PMID 39707188›Full record

ArticleMolecular medicine (Cambridge, Mass.)2024

Crosstalk between CD180-overexpression macrophages and glioma cells worsens patient survival through malignant phenotype promotion and immunosuppressive regulation.

Wen Wang, Junsheng Li, Qiheng He, Chenglong Liu, Zhiyao Zheng, Bojian Zhang, Siqi Mou, Wei Sun, Jizong Zhao

Abstract read
In one paragraph

Article in Molecular medicine (Cambridge, Mass.), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 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

9 authors.

Wen Wang *Department of Neurosurgery, Beijing Tiantan Hospital, Capital Medical University, No. 119 Nan Si Huan Xi Road, Fengtai District, Beijing, 100070, China.
Junsheng Li *Department of Neurosurgery, Beijing Tiantan Hospital, Capital Medical University, No. 119 Nan Si Huan Xi Road, Fengtai District, Beijing, 100070, China.
Qiheng He *Department of Neurosurgery, Beijing Tiantan Hospital, Capital Medical University, No. 119 Nan Si Huan Xi Road, Fengtai District, Beijing, 100070, China.
Chenglong LiuDepartment of Neurosurgery, Beijing Tiantan Hospital, Capital Medical University, No. 119 Nan Si Huan Xi Road, Fengtai District, Beijing, 100070, China.
Zhiyao ZhengDepartment of Neurosurgery, Beijing Tiantan Hospital, Capital Medical University, No. 119 Nan Si Huan Xi Road, Fengtai District, Beijing, 100070, China.
Bojian ZhangDepartment of Neurosurgery, Beijing Tiantan Hospital, Capital Medical University, No. 119 Nan Si Huan Xi Road, Fengtai District, Beijing, 100070, China.
Siqi MouDepartment of Neurosurgery, Beijing Tiantan Hospital, Capital Medical University, No. 119 Nan Si Huan Xi Road, Fengtai District, Beijing, 100070, China.
Wei SunDepartment of Neurosurgery, Beijing Tiantan Hospital, Capital Medical University, No. 119 Nan Si Huan Xi Road, Fengtai District, Beijing, 100070, China.
Jizong ZhaoDepartment of Neurosurgery, Beijing Tiantan Hospital, Capital Medical University, No. 119 Nan Si Huan Xi Road, Fengtai District, Beijing, 100070, China. zhaojizong@bjtth.org.

Funding

National Natural Science Foundation of China 82102757
6 · The paper itself

Abstract

backgroundUnderstanding the molecular mechanisms in immunosuppressive regulation is crucial for improving immunotherapeutic strategies. Macrophages, the major immune cells in tumor microenvironment (TME), play a dual role in tumor progression. CD180, primarily expressed in macrophages, remains unclear and requires further investigation.

methodsRNA-seq data were obtained to analyze CD180 expression in gliomas and assess its prognostic value. The comprehensive immune infiltration analysis was performed. Single-cell RNA-seq (scRNA-seq) data were used to examine CD180 expression distribution at the cellular level. CD180-overexpression macrophages were co-cultured with three glioma cell lines. The effects on glioma cell behavior were evaluated through qRT-PCR, Western blot, CCK-8 assay, EdU assay, Transwell assay, TUNEL assay, and flow cytometry. Differentially expressed genes (DEGs) and their potential biological functions were analyzed between different CD180 expression groups. Consensus clustering was used to identify CD180-related glioma subtypes.

resultsCD180 was significantly upregulated in glioma samples and associated with poor prognosis. High CD180 expression was correlated with increased immune cell infiltration, particularly macrophages, and elevated levels of immune checkpoints. Analysis of scRNA-seq data revealed the predominant expression of CD180 in macrophages within the glioma TME. In vitro experiments demonstrated that CD180-overexpression macrophages promoted glioma cell proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT), while decreasing apoptosis. Mutations in TP53 and PTEN were significantly more prevalent in the high CD180 expression group. We identified nine chemotherapeutic agents that were more effective in glioma patients with high CD180 expression. Additionally, two CD180-related glioma subtypes with distinct prognosis were identified.

conclusionsThis study confirmed the prognostic role of CD180 in glioma and its involvement in immunosuppressive regulation and malignant phenotype promotion. Therefore, CD180 was considered as a promising target for immunotherapeutic strategies in glioma treatment.

Indexed as

Gene Expression Regulation, NeoplasticGliomaMacrophagesTumor MicroenvironmentAntigens, CDBrain NeoplasmsCell Line, TumorCell ProliferationHumansPhenotypePrognosisAntigens, CDBiomarkerCD180GliomaImmunotherapyMacrophage

Identifiers

PMID39707188
PMCPMC11660626

What Socratic 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 Socratic graph.