Evidence map›Paper›PMID 41315804›Full record

ArticleScientific reports2025

RGS20 reduces glioma stemness and temozolomide resistance by intrinsically inhibiting the WNT/β-catenin signaling pathway.

Yang Xie, Qi Li, Yecheng Ma, Yongchang Yang, Xingyu Jin, Tailong Yi, Xianglian Ge, Xing Xu, Xuejun Yang, Qiang Huang and 6 more

Abstract read
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

16 authors.

Yang Xie *Department of Biochemistry and Molecular Biology, Key Laboratory of Cancer Prevention and Therapy, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Tianjin's Clinical Research Center for Cancer, Tianjin, 300060, China.
Qi Li *Department of Biochemistry and Molecular Biology, Key Laboratory of Cancer Prevention and Therapy, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Tianjin's Clinical Research Center for Cancer, Tianjin, 300060, China.
Yecheng Ma *Department of Biochemistry and Molecular Biology, Key Laboratory of Cancer Prevention and Therapy, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Tianjin's Clinical Research Center for Cancer, Tianjin, 300060, China.
Yongchang YangDepartment of Biochemistry and Molecular Biology, Key Laboratory of Cancer Prevention and Therapy, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Tianjin's Clinical Research Center for Cancer, Tianjin, 300060, China.
Xingyu JinDepartment of Biochemistry and Molecular Biology, Key Laboratory of Cancer Prevention and Therapy, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Tianjin's Clinical Research Center for Cancer, Tianjin, 300060, China.
Tailong YiDepartment of Biochemistry and Molecular Biology, Key Laboratory of Cancer Prevention and Therapy, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Tianjin's Clinical Research Center for Cancer, Tianjin, 300060, China.
Xianglian GeDepartment of Biochemistry and Molecular Biology, Key Laboratory of Cancer Prevention and Therapy, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Tianjin's Clinical Research Center for Cancer, Tianjin, 300060, China.
Xing XuDepartment of Biochemistry and Molecular Biology, Key Laboratory of Cancer Prevention and Therapy, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Tianjin's Clinical Research Center for Cancer, Tianjin, 300060, China.
Xuejun YangDepartment of Neurosurgery, Beijing Tsinghua Changgung Hospital, Tsinghua University, Beijing, 100000, China.
Qiang HuangDepartment of Neurosurgery, Tianjin Medical University General Hospital, Tianjin, 300052, China.
Yalin LuDepartment of Neuro-Oncology and Neurosurgery, Key Laboratory of Cancer Prevention and Therapy, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Tianjin, 300060, China.
Peng LiDepartment of Neuro-Oncology and Neurosurgery, Key Laboratory of Cancer Prevention and Therapy, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Tianjin, 300060, China.
Wenliang LiDepartment of Neuro-Oncology and Neurosurgery, Key Laboratory of Cancer Prevention and Therapy, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Tianjin, 300060, China.
Xiaoguang WangDepartment of Neuro-Oncology and Neurosurgery, Key Laboratory of Cancer Prevention and Therapy, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Tianjin, 300060, China.
Yingzhe PiaoDepartment of Neuro-Oncology and Neurosurgery, Key Laboratory of Cancer Prevention and Therapy, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Tianjin, 300060, China. 13602132633@163.com.ORCID 0009-0008-6676-3752
Xun JinDepartment of Biochemistry and Molecular Biology, Key Laboratory of Cancer Prevention and Therapy, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Tianjin's Clinical Research Center for Cancer, Tianjin, 300060, China. jinx2354@163.com.ORCID 0000-0002-1550-2199

Funding

National Natural Science Foundation of China 82273100
6 · The paper itself

Abstract

G protein-coupled receptors (GPCRs) play a pivotal role in maintaining the stemness of both normal and cancer stem cells. However, the function of the regulator of G protein signaling (RGS) family, particularly in tumor stem cells, remains poorly under-stood. Through bioinformatics analysis of clinical data, we identified RGS20 as a potential regulator of glioma stemness and temozolomide (TMZ) resistance, which may significantly influence patient prognosis. Subsequent in vitro and in vivo experiments demonstrated that RGS20 inhibition markedly enhanced tumor sphere formation and upregulated stem cell markers by intrinsically activating the WNT/β-catenin signaling pathway, thereby promoting tumorigenesis and ultimately leading to TMZ resistance. Furthermore, in human glioblastoma specimens, β-catenin signaling associated with low RGS20 expression was significantly enriched in hypoxic regions, suggesting that this mechanism may support the maintenance of glioma stem cells (GSCs) and drive TMZ resistance within the hypoxic niche. Our findings reveal that low RGS20 expression sustains WNT/β-catenin signaling in a ligand-reduced manner within hypoxic niches, unveiling a novel intracellular mechanism that drives glioma progression. Targeting this mechanism could provide new therapeutic strategies for glioma treatment.

Indexed as

Brain NeoplasmsDrug Resistance, NeoplasmGliomaNeoplastic Stem CellsRGS ProteinsTemozolomideWnt Signaling PathwayAnimalsAntineoplastic Agents, Alkylatingbeta CateninCell Line, TumorGene Expression Regulation, NeoplasticHumansMiceXenograft Model Antitumor AssaysAntineoplastic Agents, Alkylatingbeta CateninRGS ProteinsTemozolomideHypoxiaRGS20StemnessTMZ-resistanceWNT/β-catenin signaling pathway

Identifiers

PMID41315804
PMCPMC12753681

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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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 Socratic graph.