Evidence map›Paper›PMID 34120140›Full record

ArticleCell death & disease2021

G-protein-coupled receptor GPR17 inhibits glioma development by increasing polycomb repressive complex 1-mediated ROS production.

Huiqing Liu, Rui Xing, Zhimin Ou, Junying Zhao, Guolin Hong, Tong-Jin Zhao, Ying Han, Ying Chen

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
3.3field-weighted citation impact, top 7% 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

17 citing papers in PubMed, 29 citations in OpenAlex.

  1. Article
  2. Article
  3. The GPCR Connection: Linking Alzheimer's Disease and Glioblastoma.Journal of cellular and molecular medicine · 2026
    Review
  4. Review
  5. Review
  6. Article
  7. Review
  8. Article
  9. Review
  10. Article
  11. Review
  12. KLF9 deficiency protects the heart from inflammatory injury triggered by myocardial infarction.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2023
    Article
  13. Article
  14. Article
  15. SP and KLF Transcription Factors in Cancer Metabolism.International journal of molecular sciences · 2022
    Review
  16. Article
  17. 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

8 authors at 3 institutions in 1 country.

Huiqing Liu *State Key Laboratory of Cellular Stress Biology, School of Life Sciences, Xiamen University, Xiamen, Fujian Province, China.
Rui Xing *State Key Laboratory of Cellular Stress Biology, School of Life Sciences, Xiamen University, Xiamen, Fujian Province, China.
Zhimin Ou *State Key Laboratory of Cellular Stress Biology, School of Life Sciences, Xiamen University, Xiamen, Fujian Province, China.
Junying ZhaoState Key Laboratory of Cellular Stress Biology, School of Life Sciences, Xiamen University, Xiamen, Fujian Province, China.
Guolin HongThe Department of Laboratory Medicine, The First Affiliated Hospital of Xiamen University, Xiamen, Fujian Province, China.
Tong-Jin ZhaoInstitute of Metabolism and Integrative Biology, Fudan University, Shanghai, China.
Ying HanThe Department of Laboratory Medicine, The First Affiliated Hospital of Xiamen University, Xiamen, Fujian Province, China. hanyingatu@163.com.
Ying ChenState Key Laboratory of Cellular Stress Biology, School of Life Sciences, Xiamen University, Xiamen, Fujian Province, China. yingchen@xmu.edu.cn.
Xiamen University · CNFirst Affiliated Hospital of Xiamen University · CNFudan University · CN

Funding

National Natural Science Foundation of China (National Science Foundation of China) 31771122National Natural Science Foundation of China (National Science Foundation of China) 81601080National Natural Science Foundation of China (National Science Foundation of China) 81772287
6 · The paper itself

Abstract

Glioma is the most common primary tumor in the central nervous system. However, the development of glioma and effective therapeutic strategies remain elusive. Here, we identify GPR17 as a potential target to treat glioma. Data mining with human LGG and GBM samples reveals that GPR17 is negatively correlated with glioma development. Overexpressing GPR17 inhibits glioma cell proliferation and induces apoptosis by raising ROS levels. GPR17-overexpressing glioma cells are less tumorigenic in the brain than in control cells. Mechanistically, GPR17 inhibits the transcription of RNF2, a key component in the PRC1 complex, through cAMP/PKA/NF-κB signaling, leading to reduced histone H2A monoubiquitination. ChIP-Seq and RNA-Seq analyses reveal KLF9 as a direct target of RNF2. KLF9 mediates the functions of GPR17 and RNF2 in glioma cells. Furthermore, activation of GPR17 by its agonist inhibits glioma formation. Our findings have thus identified GPR17 as a key regulator of glioma development and a potential therapeutic target for gliomas.

Indexed as

AnimalsApoptosisBrain NeoplasmsCell ProliferationCell Transformation, NeoplasticGene Expression Regulation, NeoplasticGliomaHEK293 CellsHumansMaleMiceMice, Inbred BALB CMice, NudePolycomb Repressive Complex 1Reactive Oxygen SpeciesReceptors, G-Protein-CoupledGPR17 protein, humanPolycomb Repressive Complex 1Reactive Oxygen SpeciesReceptors, G-Protein-Coupled

Identifiers

PMID34120140
PMCPMC8197764
OpenAlexW3170646794

What OpenQuestion holds

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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.