Evidence map›Paper›PMID 38347095›Full record

ArticleBritish journal of cancer2024

ABCC4 suppresses glioblastoma progression and recurrence by restraining cGMP-PKG signalling.

Jung-Ying Chiang, Sung-Tai Wei, Huan-Jui Chang, Der-Cherng Chen, Hwai-Lee Wang, Fu-Ju Lei, Kai-Yu Wei, Yen-Chih Huang, Chi-Chung Wang, Chia-Hung Hsieh

Open access · greenAbstract read
In one paragraph

Article in British journal of cancer, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
1.7field-weighted citation impact, top 14% 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

3 citing papers in PubMed, 6 citations in OpenAlex.

  1. Article
  2. Review
  3. 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

10 authors at 4 institutions in 1 country.

Jung-Ying Chiang *Graduate Institute of Biomedical Sciences, China Medical University, Taichung, Taiwan.
Sung-Tai Wei *Division of Neurosurgery, Asia University Hospital, Taichung, Taiwan.
Huan-Jui ChangGraduate Institute of Biomedical Sciences, China Medical University, Taichung, Taiwan.
Der-Cherng ChenDepartment of Neurosurgery, China Medical University and Hospital, Taichung, Taiwan.
Hwai-Lee WangGraduate Institute of Biomedical Sciences, China Medical University, Taichung, Taiwan.
Fu-Ju LeiGraduate Institute of Clinical Medical Sciences, China Medical University, Taichung, Taiwan.
Kai-Yu WeiGraduate Institute of Biomedical Sciences, China Medical University, Taichung, Taiwan.
Yen-Chih HuangDepartment of Medical Imaging, China Medical University and Hospital, Taichung, Taiwan.
Chi-Chung WangGraduate Institute of Biomedical and Pharmaceutical Science, Fu Jen Catholic University, New Taipei, Taiwan.
Chia-Hung HsiehGraduate Institute of Biomedical Sciences, China Medical University, Taichung, Taiwan. chhsiehcmu@mail.cmu.edu.tw.ORCID 0000-0002-4364-0994
China Medical University · TWAsia University · TWFu Jen Catholic University · TWMingDao University · TW

Funding

China Medical University Hospital (CMUH) CMU112-MF-34China Medical University Hospital (CMUH) DMR-112-079China Medical University Hospital (CMUH) DMR-112-133China Medical University Hospital (CMUH) DMR-113-122
6 · The paper itself

Abstract

backgroundCyclic nucleotides are critical mediators of cellular signalling in glioblastoma. However, the clinical relevance and mechanisms of regulating cyclic nucleotides in glioblastoma progression and recurrence have yet to be thoroughly explored.

methodsIn silico, mRNA, and protein level analyses identified the primary regulator of cyclic nucleotides in recurrent human glioblastoma. Lentiviral and pharmacological manipulations examined the functional impact of cyclic nucleotide signalling in human glioma cell lines and primary glioblastoma cells. An orthotopic xenograft mice model coupled with aspirin hydrogels verified the in vivo outcome of targeting cyclic nucleotide signalling.

resultsElevated intracellular levels of cGMP, instead of cAMP, due to a lower substrate efflux from ATP-binding cassette sub-family C member 4 (ABCC4) is engaged in the recurrence of glioblastoma. ABCC4 gene expression is negatively associated with recurrence and overall survival outcomes in glioblastoma specimens. ABCC4 loss-of-function activates cGMP-PKG signalling, promoting malignancy in glioblastoma cells and xenografts. Hydrogels loaded with aspirin, inhibiting glioblastoma progression partly by upregulating ABCC4 expressions, augment the efficacy of standard-of-care therapies in orthotopic glioblastoma xenografts.

conclusionABCC4, repressing the cGMP-PKG signalling pathway, is a tumour suppressor in glioblastoma progression and recurrence. Aspirin hydrogels impede glioblastoma progression through ABCC4 restoration and constitute a viable translational approach.

Indexed as

Cyclic AMPGlioblastomaAnimalsAspirinATP-Binding Cassette, Sub-Family C ProteinsCyclic GMPHumansHydrogelsMiceNeoplasm Recurrence, LocalNucleotides, CyclicABCC4 protein, humanAspirinATP-Binding Cassette, Sub-Family C ProteinsCyclic AMPCyclic GMPHydrogelsNucleotides, Cyclic

Identifiers

PMID38347095
PMCPMC11014854
OpenAlexW4391766864

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.