Evidence map›Paper›PMID 41353504›Full record

ArticleScientific reports2025

Restoring the glioblastoma tumor microenvironment by targeting C5a with the antagonist W54011.

Yoojung Oh, Jihwan Yoo, Dongkyu Lee, Bongki Ko, Jun Pyo Hong, Ju Hyung Moon, Eui Hyun Kim, Jong Hee Chang, Yong-Chul Kim, Seok-Gu Kang

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Review
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.

Yoojung Oh *Department of Neurosurgery, Brain Tumor Center, Severance Hospital, Yonsei University College of Medicine, 50-1 Yonsei-ro, Seodaemun-gu, Seoul, 03722, Republic of Korea.
Jihwan Yoo *Department of Neurosurgery, Gangnam Severance Hospital, Yonsei University College of Medicine, Seoul, 06273, Republic of Korea.
Dongkyu LeeDepartment of Neurosurgery, Brain Tumor Center, Severance Hospital, Yonsei University College of Medicine, 50-1 Yonsei-ro, Seodaemun-gu, Seoul, 03722, Republic of Korea.
Bongki KoSchool of Life Sciences, Gwangju Institute of Science & Technology, 123 Cheomdangwagi-ro, Buk-gu, Gwangju, 61005, Republic of Korea.
Jun Pyo HongDepartment of Neurosurgery, Brain Tumor Center, Severance Hospital, Yonsei University College of Medicine, 50-1 Yonsei-ro, Seodaemun-gu, Seoul, 03722, Republic of Korea.
Ju Hyung MoonDepartment of Neurosurgery, Brain Tumor Center, Severance Hospital, Yonsei University College of Medicine, 50-1 Yonsei-ro, Seodaemun-gu, Seoul, 03722, Republic of Korea.ORCID 0000-0002-8925-5821
Eui Hyun KimDepartment of Neurosurgery, Brain Tumor Center, Severance Hospital, Yonsei University College of Medicine, 50-1 Yonsei-ro, Seodaemun-gu, Seoul, 03722, Republic of Korea.
Jong Hee ChangDepartment of Neurosurgery, Brain Tumor Center, Severance Hospital, Yonsei University College of Medicine, 50-1 Yonsei-ro, Seodaemun-gu, Seoul, 03722, Republic of Korea.ORCID 0000-0003-1509-9800
Yong-Chul KimSchool of Life Sciences, Gwangju Institute of Science & Technology, 123 Cheomdangwagi-ro, Buk-gu, Gwangju, 61005, Republic of Korea. yongchul@gist.ac.kr.
Seok-Gu KangDepartment of Neurosurgery, Brain Tumor Center, Severance Hospital, Yonsei University College of Medicine, 50-1 Yonsei-ro, Seodaemun-gu, Seoul, 03722, Republic of Korea. seokgu9@gmail.com.ORCID 0000-0001-5676-2037

Funding

Korea Health Industry Development Institute (KHIDI) RS-2024-00438443Ministry of Science, ICT and Future Planning (MSIP) NRF2022M3C1A309202211
6 · The paper itself

Abstract

Glioblastoma (GBM) poses a serious challenge due to its aggressive nature and poor prognosis. Tumor mesenchymal stem-like cells (tMSLCs) secrete complement component 5a (C5a), altering the tumor microenvironment (TME) and promoting tumor progression. This study investigated W54011, a C5a antagonist, to counteract C5a-induced malignancy in GBM tumorspheres. We assessed GBM tissues for C5a receptor 1 (C5aR1) expression using gene profiling and survival analysis. GBM tumorspheres were cultured in C5a-enriched conditioned medium (CM) from tMSLCs to induce tumor stimulation. We evaluated proliferation, invasion, and stemness of GBM tumorspheres using WST/ATP, matrigel invasion assay, and limiting dilution assays. Results were validated via western blotting and RNA sequencing. Additionally, findings were corroborated in an in vivo xenograft mouse model. High C5aR1 expression correlated with increased TME, inflammation-related gene expression, and poorer patient outcomes. CM treatment increased GBM tumorsphere proliferation, invasion, and stemness, which were reversed by W54011. CM also induced the epithelial-mesenchymal transition, whereas W54011 restored spherical morphology and induced apoptosis. In xenograft models, CM-treated GBM tumorspheres led to larger tumors and decreased survival, whereas W54011 decreased tumor size and improved survival. This study suggests a potential role for C5a in GBM progression and supports further investigation of W54011 as a therapeutic candidate.

Indexed as

Brain NeoplasmsComplement C5aGlioblastomaTumor MicroenvironmentAnimalsApoptosisCell Line, TumorCell ProliferationEpithelial-Mesenchymal TransitionFemaleGene Expression Regulation, NeoplasticHumansMaleMiceReceptor, Anaphylatoxin C5aXenograft Model Antitumor AssaysC5AR1 protein, humanComplement C5aReceptor, Anaphylatoxin C5aComplement component 5aGlioblastomaTumor mesenchymal stem-like cellTumor microenvironmentTumorsphereW54011

Identifiers

PMID41353504
PMCPMC12738741

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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 OpenQuestion graph.