Evidence map›Paper›PMID 40520103›Full record

ArticleiScience2025

TAMs-specific ARF1 inhibition reprograms glioma microenvironment and enhances the therapeutic effect of oncolytic adenovirus.

Tao Cao, Tong Hao, Xiaoru Zhang, Bo Chen, Hongxuan Zhang, Luocheng Shao, Wenqiao He, Bingnan Li, Qihao Zheng, Peng Ji and 1 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in iScience, 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

11 authors.

Tao CaoDepartment of Cell Biology, National Translational Science Center for Molecular Medicine, Fourth Military Medical University, Xi'an, Shaanxi Province 710032, China.
Tong HaoDepartment of Burns and Cutaneous Surgery, Burn Center of PLA, The First Affiliated Hospital of Air Force Medical University, Xi'an, Shaanxi Province 710032, China.
Xiaoru ZhangNuclear Medicine Laboratory, Tangshan People's Hospital, Tangshan, Hebei Province 063000, China.
Bo ChenSchool of Pharmaceutical Science, Wenzhou Medical University, Wenzhou, Zhejiang Province 325000, China.
Hongxuan ZhangThe First Clinical School, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang Province 325000, China.
Luocheng ShaoDepartment of Wound Repair, Wound Repair and Regenerative Medicine Center, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang Province 325000, China.
Wenqiao HeDepartment of Wound Repair, Wound Repair and Regenerative Medicine Center, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang Province 325000, China.
Bingnan LiDepartment of Wound Repair, Wound Repair and Regenerative Medicine Center, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang Province 325000, China.
Qihao ZhengThe First Clinical School, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang Province 325000, China.
Peng JiDepartment of Burns and Cutaneous Surgery, Burn Center of PLA, The First Affiliated Hospital of Air Force Medical University, Xi'an, Shaanxi Province 710032, China.
Ke TaoDepartment of Wound Repair, Wound Repair and Regenerative Medicine Center, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang Province 325000, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Gliomas, characterized by their robust immunosuppressive microenvironment, pose a significant challenge to the efficacy of immunotherapies. The cGas/STING signaling pathway is emerging as a promising target for cancer immunotherapy. The inhibition of ADP-ribosylation factor 1 (ARF1), a pivotal regulator within cGas/STING signaling pathway, has been shown to enhance the activation cGas/STING. We investigated the impact of macrophage-specific ARF1 suppression on the phenotype of tumor-associated macrophages (TAMs) and the subsequent tumor specific immune response. Our findings reveal that targeted downregulation of ARF1 in TAMs substantially amplifies the immune response induced by oncolytic adenoviruses, effectively reprograms these macrophages, and bolsters anti-tumor immunity. The use of oncolytic adenoviruses armed with ARF1 knockdown elements has been demonstrated to exert a significant suppressive effect on glioma growth through the concerted action of multiple pathways and effectively elicit immune memory, thereby enhancing the survival rates of tumor bearing mice and preventing tumor recurrence.

Indexed as

CancerImmunologyMolecular biology

Identifiers

PMID40520103
PMCPMC12164047

What OpenQuestion holds

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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.