Evidence map›Paper›PMID 42135837›Full record

ArticleJournal of translational medicine2026

KLRG1 silencing increases the efficacy of CAR NK cell therapy against colon cancer via SHP-2/ZAP-70/NF-κB signal pathway.

Yiran Chen, Muhammad Asad Farooq, Xinhui Hui, Yunhe Huang, Yue Hu, Min Xue, Iqra Ajmal, Yaojun Ren, Yuzhou Ji, Chen Wang and 1 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of translational medicine, 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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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.

Yiran Chen *Shanghai Key Laboratory of Regulatory Biology, School of Life Sciences, East China Normal University, 500 Dongchuan Road, Shanghai, 200241, China.
Muhammad Asad Farooq *Shanghai Key Laboratory of Regulatory Biology, School of Life Sciences, East China Normal University, 500 Dongchuan Road, Shanghai, 200241, China.
Xinhui HuiThe First Affiliated Hospital, State Key Laboratory of Respiratory Diseases, Guangzhou Medical University, Guangzhou, 510120, China.
Yunhe HuangShanghai Key Laboratory of Regulatory Biology, School of Life Sciences, East China Normal University, 500 Dongchuan Road, Shanghai, 200241, China.
Yue HuShanghai Key Laboratory of Regulatory Biology, School of Life Sciences, East China Normal University, 500 Dongchuan Road, Shanghai, 200241, China.
Min XueShanghai Key Laboratory of Regulatory Biology, School of Life Sciences, East China Normal University, 500 Dongchuan Road, Shanghai, 200241, China.
Iqra AjmalShanghai Key Laboratory of Regulatory Biology, School of Life Sciences, East China Normal University, 500 Dongchuan Road, Shanghai, 200241, China.
Yaojun RenCollege of Life Science, Xinjiang Normal University, Urumqi, China.
Yuzhou JiShanghai Key Laboratory of Regulatory Biology, School of Life Sciences, East China Normal University, 500 Dongchuan Road, Shanghai, 200241, China.
Chen WangDepartment of Oncology, Xin Hua Hospital, School of Medicine, Shanghai Jiao Tong University, 1665 Kongjiang Road, Shanghai, 200092, China. wangchenchina@126.com.
Wenzheng JiangShanghai Key Laboratory of Regulatory Biology, School of Life Sciences, East China Normal University, 500 Dongchuan Road, Shanghai, 200241, China. wzjiang@bio.ecnu.edu.cn.ORCID 0000-0003-4999-4168

Funding

Key Technologies Research and Development Program 2021YFF0702401National Natural Science Foundation of China 81771306Natural Science Foundation of Shanghai Municipality 24ZR1449500NMPA Key Laboratory for Quality Control of Therapeutic Monoclonal Antibodies 2023-DK-01Science and Technology Commission of Shanghai Municipality 201409002900Science and Technology Commission of Shanghai Municipality 21S11906200
6 · The paper itself

Abstract

backgroundNK cells are the core cells of the innate immune system, which can kill cancer cells non-specifically and almost do not cause immune rejection or neurotoxicity, thereby enabling broad application in immune cell therapy. The KLRG1/Cadherin signaling axis has been reported to inhibit the anti-tumor response of NK cells. However, the mechanism by which KLRG1 regulates CAR NK cell function remains unclear.

methodsTo investigate the regulatory role of KLRG1 in CAR NK cell function, we constructed a KLRG1-knockdown NKG2D-CAR construct using gene-silencing techniques and transduced it into NK92 cells. Through in vitro and in vivo experiments, we examined the effects of KLRG1-interfered NKG2D-CAR NK cells on colorectal cancer.

resultsOur findings suggest that KLRG1 knockdown enhanced the anti-colon cancer cytotoxicity of CAR NK cells by increasing the expression of CD69, CD107a, IFN-γ, GzmB, Perforin, and TNF-α both in vitro and in vivo. Additionally, KLRG1 deficiency improved the proliferation and survival of CAR NK cells while reducing their depletion. Mechanically, KLRG1 regulates CAR NK cell function through the ZAP-70/NF-κB signaling axis.

conclusionOur study demonstrated that down-regulation of KLRG1 enhanced the anti-tumor activity of CAR NK cells, providing a new idea for CAR NK cell therapy.

Indexed as

Colonic NeoplasmsGene SilencingImmunotherapy, AdoptiveKiller Cells, NaturalLectins, C-TypeNF-kappa BReceptors, ImmunologicSignal TransductionAnimalsCell Line, TumorHumansMiceNK Cell Lectin-Like Receptor Subfamily KKLRG1 protein, humanLectins, C-TypeNF-kappa BNK Cell Lectin-Like Receptor Subfamily KReceptors, ImmunologicCAR NKColon cancerKLRG1NF-κBNKG2DZAP-70

Identifiers

PMID42135837
PMCPMC13343634

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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.