Evidence map›Paper›PMID 41560319›Full record

ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2026

Depletion of the RNA-Editing Enzyme ADAR1 Invigorates the Antitumor Immunity of NK Cells.

Shuhan Chen, Di Lu, Rukang Liang, Weikeng Tan, Erming Zhao, Sihuang Wu, Xintong Li, Yulong Song, Miaojian Wan, Xiaoyuan Xie and 2 more

Abstract read
In one paragraph

Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Review
  2. Depletion of the RNA-Editing Enzyme ADAR1 Invigorates the Antitumor Immunity of NK Cells.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
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.

Shuhan ChenBiotherapy Center, The Third Affiliated Hospital, Sun Yat-sen University, Guangzhou, China.
Di LuBiotherapy Center, The Third Affiliated Hospital, Sun Yat-sen University, Guangzhou, China.
Rukang LiangBiotherapy Center, The Third Affiliated Hospital, Sun Yat-sen University, Guangzhou, China.
Weikeng TanBiotherapy Center, The Third Affiliated Hospital, Sun Yat-sen University, Guangzhou, China.
Erming ZhaoBiotherapy Center, The Third Affiliated Hospital, Sun Yat-sen University, Guangzhou, China.
Sihuang WuBiotherapy Center, The Third Affiliated Hospital, Sun Yat-sen University, Guangzhou, China.
Xintong LiBiotherapy Center, The Third Affiliated Hospital, Sun Yat-sen University, Guangzhou, China.
Yulong SongState Key Laboratory of Respiratory Disease, The Affiliated Panyu Central Hospital of Guangzhou Medical University, State Key Laboratory of Respiratory Disease, GMU-GIBH Joint School of Life Sciences, Guangdong Provincial Key Laboratory of Protein Modification and Degradation/Disease, The Guangdong-Hong Kong-Macau Joint Laboratory for Cell Fate Regulation and Diseases, Guangzhou Medical University, Guangzhou, Guangdong, 511436, China.
Miaojian WanDepartment of Dermatology and Cosmetic Surgery, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, China.
Xiaoyuan XieDepartment of Dermatology and Cosmetic Surgery, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, China.
Qi ZhangBiotherapy Center, The Third Affiliated Hospital, Sun Yat-sen University, Guangzhou, China.
Qiuli LiuBiotherapy Center, The Third Affiliated Hospital, Sun Yat-sen University, Guangzhou, China.ORCID https://orcid.org/0000-0002-8090-8718

Funding

Fundamental Research Funds for Central University, Sun Yat-sen University 24ykqb006Guangdong Basic and Applied Basic Research Foundation 2023A1515011081National Key Research and Development Program of China 2024YFA1107200National Natural Science Foundation of China 82370629:81971526National Natural Science Foundation of China 82425010National Natural Science Foundation of China 92269107Science and Technology Program of Guangzhou 202201020398Science and Technology Program of Guangzhou 2024B03J1241
6 · The paper itself

Abstract

Functional exhaustion and inefficient tumor infiltration rates limit the effectiveness of natural killer (NK) cell-based cancer immunotherapy. Although the role of adenosine deaminase acting on RNA 1 (ADAR1) in immune cells and tumorigenesis is gradually gaining attention, its role in NK cells is elusive. In this study, we find that ADAR1 expression level is increased in peripheral blood (PB)-NK cells from patients with melanoma, concurrently exhibiting impaired tumor killing capacity. ADAR1-knockdown NK cells show enhanced antitumor activity in vitro and in vivo. Compared with ADAR1

Indexed as

Adenosine DeaminaseKiller Cells, NaturalMelanomaRNA-Binding ProteinsAnimalsHumansMiceMice, KnockoutRNA EditingADAR1 protein, mouseADAR protein, humanAdenosine DeaminaseRNA-Binding ProteinsADAR1anti‐tumor immunityCD38natural killer cells

Identifiers

PMID41560319
PMCPMC13205767

What OpenQuestion holds

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Registered trials

None linked

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.