Evidence map›Paper›PMID 38898023›Full record

ArticleCell death & disease2024

CXCR7 activation evokes the anti-PD-L1 antibody against glioblastoma by remodeling CXCL12-mediated immunity.

Chan-Chuan Liu, Wen-Bin Yang, Chia-Hung Chien, Cheng-Lin Wu, Jian-Ying Chuang, Pin-Yuan Chen, Jui-Mei Chu, Siao Muk Cheng, Li-Ying Qiu, Yung-Chieh Chang and 4 more

Abstract read
In one paragraph

Article in Cell death & disease, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing 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

13 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
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

14 authors.

Chan-Chuan LiuNational Institute of Cancer Research, National Health Research Institutes, Tainan, Taiwan.
Wen-Bin YangResearch Center for Neuroscience, Taipei Medical University, Taipei, Taiwan.ORCID 0000-0002-6497-4176
Chia-Hung Chien *National Institute of Cancer Research, National Health Research Institutes, Tainan, Taiwan.
Cheng-Lin Wu *Department of Pathology, National Cheng Kung University Hospital, College of Medicine, National Cheng-Kung University, Tainan, Taiwan.
Jian-Ying ChuangResearch Center for Neuroscience, Taipei Medical University, Taipei, Taiwan.ORCID 0000-0001-5124-0643
Pin-Yuan ChenSchool of Medicine, Chang Gung University, Taoyuan, Taiwan.
Jui-Mei ChuNational Institute of Cancer Research, National Health Research Institutes, Tainan, Taiwan.
Siao Muk ChengNational Institute of Cancer Research, National Health Research Institutes, Tainan, Taiwan.
Li-Ying QiuNational Institute of Cancer Research, National Health Research Institutes, Tainan, Taiwan.
Yung-Chieh ChangNational Institute of Cancer Research, National Health Research Institutes, Tainan, Taiwan.
Daw-Yang HwangNational Institute of Cancer Research, National Health Research Institutes, Tainan, Taiwan.
Chih-Yuan HuangDivision of Neurosurgery, Department of Surgery, National Cheng Kung University Hospital, College of Medicine, National Cheng Kung University, Tainan, Taiwan.
Jung-Shun LeeDivision of Neurosurgery, Department of Surgery, National Cheng Kung University Hospital, College of Medicine, National Cheng Kung University, Tainan, Taiwan.
Kwang-Yu ChangNational Institute of Cancer Research, National Health Research Institutes, Tainan, Taiwan. kwang2@nhri.edu.tw.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The interaction between glioblastoma cells and glioblastoma-associated macrophages (GAMs) influences the immunosuppressive tumor microenvironment, leading to ineffective immunotherapies. We hypothesized that disrupting the communication between tumors and macrophages would enhance the efficacy of immunotherapies. Transcriptomic analysis of recurrent glioblastoma specimens indicated an enhanced neuroinflammatory pathway, with CXCL12 emerging as the top-ranked gene in secretory molecules. Single-cell transcriptome profiling of naïve glioblastoma specimens revealed CXCL12 expression in tumor and myeloid clusters. An analysis of public glioblastoma datasets has confirmed the association of CXCL12 with disease and PD-L1 expression. In vitro studies have demonstrated that exogenous CXCL12 induces pro-tumorigenic characteristics in macrophage-like cells and upregulated PD-L1 expression through NF-κB signaling. We identified CXCR7, an atypical receptor for CXCL12 predominantly present in tumor cells, as a negative regulator of CXCL12 expression by interfering with extracellular signal-regulated kinase activation. CXCR7 knockdown in a glioblastoma mouse model resulted in worse survival outcomes, increased PD-L1 expression in GAMs, and reduced CD8

Indexed as

B7-H1 AntigenChemokine CXCL12GlioblastomaReceptors, CXCRAnimalsBrain NeoplasmsCell Line, TumorHumansMiceSignal TransductionTumor MicroenvironmentACKR3 protein, humanB7-H1 AntigenCD274 protein, humanChemokine CXCL12CXCL12 protein, humanReceptors, CXCR

Identifiers

PMID38898023
PMCPMC11187218

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.