Evidence map›Paper›PMID 41748771›Full record

ArticleMolecular biomedicine2026

TBC1 domain family member 23 is essential for STING-mediated anti-melanoma effect.

Shenghui Niu, Guangmei Li, Pengcheng Wei, Xiang Hu, Junhong Qin, Yin Yuan, Jinrui Wang, Yingfeng Tu, Lin Zhao, Luoting Yu and 1 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Molecular biomedicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0cells of the map it votes in
0citing papers in PubMed
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1 · What the graph read from it

What it found

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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

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

11 authors.

Shenghui Niu *Key Laboratory of Birth Defects and Related Diseases of Women and Children, Department of Paediatrics, West China Second University Hospital, State Key Laboratory of Biotherapy, Sichuan University, Chengdu, 610041, China.
Guangmei Li *State Key Laboratory of Biotherapy and Cancer Center, West China Hospital, and Collaborative Innovation Center of Biotherapy, Sichuan University, Chengdu, 610041, China.
Pengcheng WeiKey Laboratory of Birth Defects and Related Diseases of Women and Children, Department of Paediatrics, West China Second University Hospital, State Key Laboratory of Biotherapy, Sichuan University, Chengdu, 610041, China.
Xiang HuState Key Laboratory of Biotherapy and Cancer Center, West China Hospital, and Collaborative Innovation Center of Biotherapy, Sichuan University, Chengdu, 610041, China.
Junhong QinKey Laboratory of Birth Defects and Related Diseases of Women and Children, Department of Paediatrics, West China Second University Hospital, State Key Laboratory of Biotherapy, Sichuan University, Chengdu, 610041, China.
Yin YuanKey Laboratory of Birth Defects and Related Diseases of Women and Children, Department of Paediatrics, West China Second University Hospital, State Key Laboratory of Biotherapy, Sichuan University, Chengdu, 610041, China.
Jinrui WangKey Laboratory of Birth Defects and Related Diseases of Women and Children, Department of Paediatrics, West China Second University Hospital, State Key Laboratory of Biotherapy, Sichuan University, Chengdu, 610041, China.
Yingfeng TuKey Laboratory of Birth Defects and Related Diseases of Women and Children, Department of Paediatrics, West China Second University Hospital, State Key Laboratory of Biotherapy, Sichuan University, Chengdu, 610041, China.
Lin ZhaoKey Laboratory of Birth Defects and Related Diseases of Women and Children, Department of Paediatrics, West China Second University Hospital, State Key Laboratory of Biotherapy, Sichuan University, Chengdu, 610041, China.
Luoting YuState Key Laboratory of Biotherapy and Cancer Center, West China Hospital, and Collaborative Innovation Center of Biotherapy, Sichuan University, Chengdu, 610041, China. yuluot@scu.edu.cn.
Da JiaKey Laboratory of Birth Defects and Related Diseases of Women and Children, Department of Paediatrics, West China Second University Hospital, State Key Laboratory of Biotherapy, Sichuan University, Chengdu, 610041, China. JiaDa@scu.edu.cn.ORCID http://orcid.org/0000-0002-2205-1998

Funding

National Key R&D Program of China 92254302
6 · The paper itself

Abstract

The innate immune cyclic GMP-AMP synthase-stimulator of interferon genes (cGAS-STING) pathway plays a central role in antitumor immune responses. Cytosolic DNA recognition by cGAS leads to cGAMP production, activating STING and downstream effectors TANK-binding kinase 1 (TBK1) and Interferon regulatory factor 3 (IRF3). This signaling induces the production of type I interferons (IFN-I) and chemokines, facilitating CD8⁺ T cell activation and recruitment to enhance antitumor immunity. The cGAS-STING pathway is critically regulated by vesicular trafficking, which governs its spatially resolved activation across multiple subcellular compartments, thereby facilitating precise control of innate immune signaling. TBC1 domain family member 23 (TBC1D23), a member of the Tre2-Bub2-Cdc16 (TBC) family, is a key regulator of intracellular vesicle transport and is required for trafficking TBK1 from endosomes to the trans-Golgi network. Although Tbc1d23 deletion impairs STING-induced IFN-I production, its physiological role in antitumor immunity remains unclear. Here, we report that high TBC1D23 expression correlates with enhanced immune infiltration and favorable prognosis in melanoma. Conversely, TBC1D23 deficiency severely impairs the STING-dependent expression of key IFN-inducible chemokines, suppresses immunostimulatory macrophage maturation, and diminishes the infiltration, activation, and cytotoxic function of tumor-antigen-specific CD8⁺ T cells. Consequently, loss of TBC1D23 accelerates melanoma progression. Our findings establish TBC1D23 as an essential regulator of STING signaling and a critical mediator of antitumor immunity.

Indexed as

GTPase-Activating ProteinsMelanomaMembrane ProteinsAnimalsCD8-Positive T-LymphocytesCell Line, TumorcGAS-STING Signaling PathwayHumansInterferon Type IMiceProtein Serine-Threonine KinasesSignal TransductionSTING ProteinGTPase-Activating ProteinsInterferon Type IMembrane ProteinsProtein Serine-Threonine KinasesSting1 protein, mouseSTING ProteinAntitumor immunityCD8+ T cell infiltrationMelanomaStimulator of interferon genes (STING) signalingTBC1 domain family member 23 (TBC1D23)

Identifiers

PMID41748771
PMCPMC12946633

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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.