Evidence map›Paper›PMID 38461299›Full record

ArticleNature communications2024

Mi-2β promotes immune evasion in melanoma by activating EZH2 methylation.

Cang Li, Zhengyu Wang, Licheng Yao, Xingyu Lin, Yongping Jian, Yujia Li, Jie Zhang, Jingwei Shao, Phuc D Tran, James R Hagman and 8 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
4.2field-weighted citation impact, top 5% of its field
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

15 citing papers in PubMed, 15 citations in OpenAlex.

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  12. Ribonuclease 1 Induces T-Cell Dysfunction and Impairs CD8Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
  13. Article
  14. Article
  15. The Roles of H3K9me3 Writers, Readers, and Erasers in Cancer Immunotherapy.International journal of molecular sciences · 2024
    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

18 authors at 12 institutions in 3 countries.

Cang Li *Skin Disease Research Institute, The 2nd Hospital and School of Medicine, Zhejiang University, Hangzhou, 310058, China.
Zhengyu Wang *Department of Pharmaceutical Sciences, College of Pharmacy, University of Arkansas for Medical Science, Little Rock, AR, 72205, USA.ORCID 0000-0003-4995-5521
Licheng Yao *State Key Laboratory of Molecular Oncology, School of Pharmaceutical Sciences, Tsinghua-Peking Center for Life Science, Tsinghua University, Beijing, 100084, China.ORCID 0000-0002-6451-8787
Xingyu LinZhuhai Yu Fan Biotechnologies Co. Ltd, Zhuhai, Guangdong, 51900, China.
Yongping JianSchool of Life Sciences, Henan University, Kaifeng, 475000, China.
Yujia LiSchool of Life Sciences, Henan University, Kaifeng, 475000, China.
Jie ZhangNational Key Laboratory for Novel Software Technology, Nanjing University, Nanjing, Jiangsu, China.ORCID 0000-0003-0242-8812
Jingwei ShaoNational & Local Joint Engineering Research Center of Targeted and Innovative Therapeutics, International Academy of Targeted Therapeutics and Innovation, College of Pharmacy, Chongqing University of Arts and Sciences, Chongqing, 402160, China.
Phuc D TranDepartment of Pharmaceutical Sciences, College of Pharmacy, University of Arkansas for Medical Science, Little Rock, AR, 72205, USA.
James R HagmanDepartment of Immunology and Genomic Medicine, National Jewish Health, Denver, CO, 80206, USA.ORCID 0000-0002-5436-8455
Meng CaoAffiliated Hospital of Integrated Traditional Chinese and Western Medicine, School of Pharmacy, Nanjing University of Chinese Medicine, Nanjing, 210023, China.
Yusheng CongKey Laboratory of Aging and Cancer Biology of Zhejiang Province, Hangzhou Normal University School of Basic Medical Sciences, Hangzhou, 310058, China.ORCID 0000-0002-1307-379X
Hong-Yu LiDepartment of Pharmaceutical Sciences, College of Pharmacy, University of Arkansas for Medical Science, Little Rock, AR, 72205, USA. lih1@uthscsa.edu.
Colin R GodingLudwig Institute for Cancer Research, Nuffield Department of Clinical Medicine, University of Oxford, Headington, Oxford, OX3 7DQ, UK. colin.goding@ludwig.ox.ac.uk.ORCID 0000-0002-1614-3909
Zhi-Xiang XuSchool of Life Sciences, Henan University, Kaifeng, 475000, China. 10140187@vip.henu.edu.cn.ORCID 0000-0002-2385-3044
Xuebin LiaoState Key Laboratory of Molecular Oncology, School of Pharmaceutical Sciences, Tsinghua-Peking Center for Life Science, Tsinghua University, Beijing, 100084, China. liaoxuebin@mail.tsinghua.edu.cn.ORCID 0000-0002-0290-894X
Xiao MiaoDepartment of Dermatology, Shuguang Hospital of Traditional Chinese Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai, 200437, China. 0000002623@shutcm.edu.cn.
Rutao CuiSkin Disease Research Institute, The 2nd Hospital and School of Medicine, Zhejiang University, Hangzhou, 310058, China. rutaocui@zju.edu.cn.ORCID 0009-0004-2590-0475
Henan University · CNUniversity of Arkansas for Medical Sciences · USZhejiang University · CNChongqing University of Arts and Sciences · CNFirst Affiliated Hospital of Jiangxi Medical College · CNHangzhou Normal University · CNKing Center · USNanjing University · CNNanjing University of Chinese Medicine · CNNational Jewish Health · USTsinghua University · CNUniversity of Oxford · GB

Funding

National Natural Science Foundation of China (National Science Foundation of China) U21A20379
6 · The paper itself

Abstract

Recent development of new immune checkpoint inhibitors has been particularly successfully in cancer treatment, but still the majority patients fail to benefit. Converting resistant tumors to immunotherapy sensitive will provide a significant improvement in patient outcome. Here we identify Mi-2β as a key melanoma-intrinsic effector regulating the adaptive anti-tumor immune response. Studies in genetically engineered mouse melanoma models indicate that loss of Mi-2β rescues the immune response to immunotherapy in vivo. Mechanistically, ATAC-seq analysis shows that Mi-2β controls the accessibility of IFN-γ-stimulated genes (ISGs). Mi-2β binds to EZH2 and promotes K510 methylation of EZH2, subsequently activating the trimethylation of H3K27 to inhibit the transcription of ISGs. Finally, we develop an Mi-2β-targeted inhibitor, Z36-MP5, which reduces Mi-2β ATPase activity and reactivates ISG transcription. Consequently, Z36-MP5 induces a response to immune checkpoint inhibitors in otherwise resistant melanoma models. Our work provides a potential therapeutic strategy to convert immunotherapy resistant melanomas to sensitive ones.

Indexed as

DNA HelicasesEnhancer of Zeste Homolog 2 ProteinImmune EvasionMelanomaAnimalsHumansImmune Checkpoint InhibitorsMethylationMiceDNA HelicasesEnhancer of Zeste Homolog 2 ProteinEZH2 protein, humanImmune Checkpoint InhibitorsMi-2beta protein, mouse

Identifiers

PMID38461299
PMCPMC10924921
OpenAlexW4392623518

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.