Evidence map›Paper›PMID 21782780›Full record

ArticleThe American journal of pathology2011

Annexin 1 released by necrotic human glioblastoma cells stimulates tumor cell growth through the formyl peptide receptor 1.

Yan Yang, Ying Liu, Xiaohong Yao, Yifang Ping, Tao Jiang, Qin Liu, Senlin Xu, Jian Huang, Haiwei Mou, Wanghua Gong and 4 more

Erratum issuedOpen access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 50 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed, 1 pooled it
1.7field-weighted citation impact, top 16% 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

50 citing papers in PubMed, 1 synthesis or guideline pooled it, 78 citations in OpenAlex.

  1. Pooled it
  2. Formyl Peptide Receptor-2-Suppressed Autophagy Promotes the Migration and Invasion of Human Glioblastoma Cells Through PI3K/Akt Signaling.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2026
    Article
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  6. TheFrontiers in immunology · 2025
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4 · The record

Corrections and comments

  • Erratum issued
    Ming Wang, Ji [corrected to Wang, Ji Ming]
5 · Who and what money

Authors and funding

14 authors at 6 institutions in 3 countries.

Yan YangLaboratory of Molecular Immunoregulation, Cancer and Inflammation Program, Center for Cancer Research, National Cancer Institute, Frederick, Maryland; College of Marine Life Sciences, Ocean University of China, Qingdao, China.
Ying Liu
Xiaohong Yao
Yifang Ping
Tao Jiang
Qin Liu
Senlin Xu
Jian Huang
Haiwei Mou
Wanghua Gong
Keqiang Chen
Xiuwu Bian
Ji Ming Wang
Ji Ming Wang
Southwest Hospital · CNFrederick National Laboratory for Cancer Research · USArmy Medical University · CNScience Applications International Corporation (United States) · USResearch Institute of General Pathology and Pathophysiology, the Russian Academy of Medical Sciences · RUShanghai Institutes for Biological Sciences · CN

Funding

CCR NIH HHS HHSN261200800001CIntramural NIH HHSNCI NIH HHS HHSN261200800001E
6 · The paper itself

Abstract

Highly malignant human gliomas overexpress the G-protein-coupled chemoattractant receptor formyl peptide receptor (FPR1), which promotes tumor progression when activated. Our previous studies demonstrated that necrotic glioblastoma cells release chemotactic agonist(s) that activate FPR1 on viable tumor cells. In the present study, we identified an FPR1 agonist released by necrotic human glioblastoma cells. Necrotic tumor cell supernatant (NecSup) contained Annexin 1 (Anx A1), a chemotatic polypeptide agonist for FPR1. Immunoabsorption of Anx A1 with a specific antibody markedly reduced the chemotactic activity of NecSup for tumor cells and diminished its capacity to promote tumor cell growth, invasion, and colony formation on soft agar. In addition, Anx A1 was present in tumor xenografts formed by human glioblastoma cells in nude mice. Anx A1 knockdown significantly reduced the tumorigenicity of glioblastoma cells in nude mice, but FPR1/Anx A1 double knockdown diminished tumor growth even further. The clinical relevance of Anx A1 in gliomas was supported by the observation that Anx A1 was more highly expressed in poorly differentiated human primary gliomas compared with lower grade tumors. Our study implicates Anx A1 as a major component in necrotic tumor cell-derived stimulants of the growth of glioblastoma via the activation of FPR1.

Indexed as

AnimalsAnnexin A1Cell Line, TumorCell ProliferationCell Transformation, NeoplasticChemotaxisGene Knockdown TechniquesGlioblastomaHumansMiceMice, NudeNecrosisNeoplasm ProteinsNeoplasm TransplantationReceptors, Formyl PeptideTransplantation, HeterologousAnnexin A1FPR1 protein, humanNeoplasm ProteinsReceptors, Formyl Peptide

Identifiers

PMID21782780
PMCPMC3157278
OpenAlexW2023885856

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.