Evidence map›Paper›PMID 40861452›Full record

ArticleFrontiers in immunology2025

GPATCH3, a splicing regulator that facilitates tumor immune evasion via the modulation of ATPase activity of DHX15.

Tingrong Ren, Gaigai Wei, Jingjing Yi, Yuqi Zhang, Haiping Zhao, Nana Wu, Huiling Zhang, Zhihan Guo, Yihan Wang, Jiating Kuang and 2 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Frontiers in immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing 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

5 citing papers in PubMed.

  1. Article
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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

12 authors.

Tingrong RenChildren's Hospital of Fudan University, National Children's Medical Center, and Shanghai Key Laboratory of Medical Epigenetics, International Co-laboratory of Medical Epigenetics and Metabolism, Ministry of Science and Technology, Institutes of Biomedical Sciences, Fudan University, Shanghai, China.
Gaigai WeiChildren's Hospital of Fudan University, National Children's Medical Center, and Shanghai Key Laboratory of Medical Epigenetics, International Co-laboratory of Medical Epigenetics and Metabolism, Ministry of Science and Technology, Institutes of Biomedical Sciences, Fudan University, Shanghai, China.
Jingjing YiChildren's Hospital of Fudan University, National Children's Medical Center, and Shanghai Key Laboratory of Medical Epigenetics, International Co-laboratory of Medical Epigenetics and Metabolism, Ministry of Science and Technology, Institutes of Biomedical Sciences, Fudan University, Shanghai, China.
Yuqi ZhangChildren's Hospital of Fudan University, National Children's Medical Center, and Shanghai Key Laboratory of Medical Epigenetics, International Co-laboratory of Medical Epigenetics and Metabolism, Ministry of Science and Technology, Institutes of Biomedical Sciences, Fudan University, Shanghai, China.
Haiping ZhaoChildren's Hospital of Fudan University, National Children's Medical Center, and Shanghai Key Laboratory of Medical Epigenetics, International Co-laboratory of Medical Epigenetics and Metabolism, Ministry of Science and Technology, Institutes of Biomedical Sciences, Fudan University, Shanghai, China.
Nana WuChildren's Hospital of Fudan University, National Children's Medical Center, and Shanghai Key Laboratory of Medical Epigenetics, International Co-laboratory of Medical Epigenetics and Metabolism, Ministry of Science and Technology, Institutes of Biomedical Sciences, Fudan University, Shanghai, China.
Huiling ZhangChildren's Hospital of Fudan University, National Children's Medical Center, and Shanghai Key Laboratory of Medical Epigenetics, International Co-laboratory of Medical Epigenetics and Metabolism, Ministry of Science and Technology, Institutes of Biomedical Sciences, Fudan University, Shanghai, China.
Zhihan GuoChildren's Hospital of Fudan University, National Children's Medical Center, and Shanghai Key Laboratory of Medical Epigenetics, International Co-laboratory of Medical Epigenetics and Metabolism, Ministry of Science and Technology, Institutes of Biomedical Sciences, Fudan University, Shanghai, China.
Yihan WangChildren's Hospital of Fudan University, National Children's Medical Center, and Shanghai Key Laboratory of Medical Epigenetics, International Co-laboratory of Medical Epigenetics and Metabolism, Ministry of Science and Technology, Institutes of Biomedical Sciences, Fudan University, Shanghai, China.
Jiating KuangChildren's Hospital of Fudan University, National Children's Medical Center, and Shanghai Key Laboratory of Medical Epigenetics, International Co-laboratory of Medical Epigenetics and Metabolism, Ministry of Science and Technology, Institutes of Biomedical Sciences, Fudan University, Shanghai, China.
Zhaoying ShengChildren's Hospital of Fudan University, National Children's Medical Center, and Shanghai Key Laboratory of Medical Epigenetics, International Co-laboratory of Medical Epigenetics and Metabolism, Ministry of Science and Technology, Institutes of Biomedical Sciences, Fudan University, Shanghai, China.
Duanwu ZhangChildren's Hospital of Fudan University, National Children's Medical Center, and Shanghai Key Laboratory of Medical Epigenetics, International Co-laboratory of Medical Epigenetics and Metabolism, Ministry of Science and Technology, Institutes of Biomedical Sciences, Fudan University, Shanghai, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Introduction: Aberrant pre-mRNA splicing is increasingly recognized as a key contributor to tumorigenesis and immune evasion. However, the regulatory factors orchestrating splicing dynamics within the tumor microenvironment (TME) remain incompletely understood. Here, we identify GPATCH3, a previously uncharacterized G-patch domain-containing protein, as a critical modulator of alternative splicing and immune regulation in cancer. Methods: We employed biochemical studies, splicing reporter assays, and transcriptomic analyses to elucidate the function of GPATCH3. Results: GPATCH3 interacts with the RNA helicase DHX15 and enhances its ATPase activity, promoting proper spliceosome disassembly. Loss of GPATCH3 led to splicing alterations, including in immunoregulatory genes such as Discussion: Our findings suggest GPATCH3 as a critical regulator that governs alternative splicing and immunosuppressive microenvironment remodeling. By modulating the splicing fidelity of key immune genes and altering their expression, GPATCH3 may facilitate immune escape and tumor progression. These results provide mechanistic insights into how RNA splicing factors interface with immune regulation and highlight GPATCH3 as a potential therapeutic target for immunomodulatory cancer therapy.

Indexed as

Adenosine TriphosphatasesDEAD-box RNA HelicasesNeoplasmsRNA HelicasesTumor EscapeAlternative SplicingAnimalsCell Line, TumorGene Expression Regulation, NeoplasticHumansMiceSpliceosomesTumor MicroenvironmentAdenosine TriphosphatasesDEAD-box RNA HelicasesRNA Helicasesalternative splicingATPase activityDEAH-box helicaseDHX15GPATCH3immune evasionsplicingtumor microenvironment

Identifiers

PMID40861452
PMCPMC12375585

What OpenQuestion holds

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LicenceCC BY
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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.