Evidence map›Paper›PMID 41809821›Full record

ArticleFrontiers in oncology2026

cGAS/STING-mediated upregulation of NKG2D ligands in LSCs contributes to enhanced sensitivity to NK cells.

Yan Ouyang, Yilin Qin, Qianmin Zhang, Pengcheng Zhu, Huifang Zhu

Abstract read
In one paragraph

Article in Frontiers in oncology, 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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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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0 citing papers in PubMed.

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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

5 authors.

Yan Ouyang *Neonatal/Pediatric Intensive Care Unit, Children's Medical Center, First Affiliated Hospital of Gannan Medical University, Ganzhou, China.
Yilin Qin *First Clinical Medical College of Gannan Medical University, Ganzhou, China.
Qianmin ZhangFirst Clinical Medical College of Gannan Medical University, Ganzhou, China.
Pengcheng ZhuFirst Clinical Medical College of Gannan Medical University, Ganzhou, China.
Huifang ZhuNeonatal/Pediatric Intensive Care Unit, Children's Medical Center, First Affiliated Hospital of Gannan Medical University, Ganzhou, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Introduction: Natural killer (NK) cells-mediated immune surveillance is essential role for tumor recognition and elimination. The binding of NK group 2 member D (NKG2D) ligands to NKG2D receptor is sufficient to activate the NK cells' cytotoxicity against targeted cells. Here we reported that the inhibition of poly (ADP-ribose) polymerase 1 (PARP1) in leukemia stem cells (LSCs) induced the expression of NKG2D ligands through the activation of DNA damage response. Methods: Flow cytometry and Quantitative real-time RT-PCR were used to detect the expression levels of NKG2D ligands on cell surface and mRNA levels in leukemia cells, respectively. Cytotoxicity assay was applied to examine the cytotoxic activity of NK cells against leukemia cells. Dual luciferase reporter (DLR) assay was employed to detect the promoter activation of NKG2D ligands. Western blotting was conducted to check the protein expression level. Results: Activated ataxia-telangiectasia mutated proteins (ATM) and ɣH2AX foci accumulation were observed under the treatment of PARP inhibitor, leading to the accumulation of damaged DNA. Subsequently, cyclic GMP-AMP synthase (cGAS) was activated, and stimulator of interferon gene (STING) was recruited to promote the downstream signal transduction via TANK-binding kinase-1 (TBK1) and transcription regulatory factor 3 (IRF3). However, the NKG2D ligands induced by PARP inhibitor was reduced in STING or IRF3-knockdown LSCs, indicating that STING and IRF3 were necessary for the regulation of NGK2D ligands in LSCs upon the DNA damage response. Discussion: These data indicated that the DNA damage response-mediated cGAS/STING/TBK1/IRF3 signalling pathway played an essential role in modulating NKG2D ligands expression in LSCs.

Indexed as

CGASDNA damage responseNK cellsNKG2D ligandsPARP1STING

Identifiers

PMID41809821
PMCPMC12967932

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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.