Evidence map›Paper›PMID 40069506›Full record

ArticleNature genetics2025

Alterations in PD-L1 succinylation shape anti-tumor immune responses in melanoma.

Long Liang, Xinwei Kuang, Yi He, Lin Zhu, Poyee Lau, Xin Li, Dingan Luo, Lan Gong, Wenbin Zhou, Fanglin Zhang and 12 more

Abstract read
In one paragraph

Article in Nature genetics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed, 1 pooled it
–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

51 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Review
  3. Article
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  5. Review
  6. Article
  7. Article
  8. International journal of molecular sciences · 2026
    Article
  9. Role of pyroptosis in melanoma: Molecular mechanisms and therapeutic potentials.Apoptosis : an international journal on programmed cell death · 2026
    Review
  10. Review
  11. Article
  12. Article
  13. Review
  14. Review
  15. Article
  16. Review
  17. Tumor cell intrinsic mechanisms of immune escape.Cell communication and signaling : CCS · 2026
    Review
  18. Article
  19. Article
  20. 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

22 authors.

Long Liang *Department of Dermatology, Xiangya Hospital & School of Life Sciences & Furong Laboratory, Central South University, Changsha, China.
Xinwei Kuang *Department of Dermatology, Xiangya Hospital & School of Life Sciences & Furong Laboratory, Central South University, Changsha, China.
Yi He *Department of Dermatology, Xiangya Hospital & School of Life Sciences & Furong Laboratory, Central South University, Changsha, China.
Lin ZhuDepartment of Dermatology, Xiangya Hospital & School of Life Sciences & Furong Laboratory, Central South University, Changsha, China.
Poyee LauDepartment of Dermatology, Xiangya Hospital & School of Life Sciences & Furong Laboratory, Central South University, Changsha, China.
Xin LiMedical Genetics & School of Life Sciences, Central South University, Changsha, China.
Dingan LuoDepartment of Dermatology, Xiangya Hospital & School of Life Sciences & Furong Laboratory, Central South University, Changsha, China.
Lan GongDepartment of Dermatology, Xiangya Hospital & School of Life Sciences & Furong Laboratory, Central South University, Changsha, China.
Wenbin ZhouDepartment of Dermatology, Xiangya Hospital & School of Life Sciences & Furong Laboratory, Central South University, Changsha, China.
Fanglin ZhangMedical Genetics & School of Life Sciences, Central South University, Changsha, China.
Xiaowei LiangDepartment of Dermatology, Xiangya Hospital & School of Life Sciences & Furong Laboratory, Central South University, Changsha, China.
Zhuofeng LiDepartment of Dermatology, Xiangya Hospital & School of Life Sciences & Furong Laboratory, Central South University, Changsha, China.
Bin HuMedical Genetics & School of Life Sciences, Central South University, Changsha, China.
Dandan LiuMedical Genetics & School of Life Sciences, Central South University, Changsha, China.
Tao DingDepartment of Statistical Science, University College London, London, UK.
Hui LiDepartment of Dermatology, Xiangya Hospital & School of Life Sciences & Furong Laboratory, Central South University, Changsha, China.
Shuang ZhaoDepartment of Dermatology, Xiangya Hospital & School of Life Sciences & Furong Laboratory, Central South University, Changsha, China.
Juan SuDepartment of Dermatology, Xiangya Hospital & School of Life Sciences & Furong Laboratory, Central South University, Changsha, China.
Mien-Chie HungGraduate Institute of Biomedical Sciences, Institute of Biochemistry and Molecular Biology, Research Center for Cancer Biology, Cancer Biology and Precision Therapeutics Center, and Center for Molecular Medicine, China Medical University, Taichung, Taiwan.ORCID http://orcid.org/0000-0003-4317-4740
Jing LiuMedical Genetics & School of Life Sciences, Central South University, Changsha, China. liujing2@sklmg.edu.cn.ORCID http://orcid.org/0000-0001-5588-3865
Hong LiuDepartment of Dermatology, Xiangya Hospital & School of Life Sciences & Furong Laboratory, Central South University, Changsha, China. hongliu1014@csu.edu.cn.ORCID http://orcid.org/0000-0001-9976-2985
Xiang ChenDepartment of Dermatology, Xiangya Hospital & School of Life Sciences & Furong Laboratory, Central South University, Changsha, China. chenxiangck@126.com.ORCID http://orcid.org/0000-0001-8187-636X

Funding

National Natural Science Foundation of China (National Science Foundation of China) 81920108004National Natural Science Foundation of China (National Science Foundation of China) 82100137National Natural Science Foundation of China (National Science Foundation of China) 82102891National Science Foundation of China | Key Programme 82130090National Science Foundation of China | Key Programme U22A20329
6 · The paper itself

Abstract

Tumors undergo metabolic reprogramming to meet the energetic, synthetic and redox demands essential for malignancy, often characterized by increased glycolysis and lactate production. However, the role of mitochondrial metabolism in tumor immunity remains unclear. The present study integrates spatial transcriptomics, bulk transcriptomics and proteomics, revealing a strong link between the metabolite succinyl-CoA and tumor immunity as well as the efficacy of anti-programmed cell death protein-1 (PD-1) therapy in patients with melanoma. Elevated succinyl-CoA levels, through α-ketoglutarate or succinate supplementation, enhanced T cell-mediated tumor elimination, both in vitro and in vivo. Mechanistically, succinylation of the ligand of PD-1 (PD-L1) at lysine 129 led to its degradation. Increased carnitine palmitoyltransferase 1A (CPT1A), identified as a succinyltransferase for PD-L1, boosted anti-tumor activity. Preclinically, bezafibrate, a hyperlipidemia drug, upregulated CPT1A and synergized with CTLA-4 monoclonal antibody to inhibit tumor growth. Clinically, higher PD-L1 and lower CPT1A levels in tumors correlated with better anti-PD-1 therapy responses, suggesting potential biomarkers for prediction of treatment efficacy.

Indexed as

B7-H1 AntigenMelanomaAnimalsBezafibrateCarnitine O-PalmitoyltransferaseCell Line, TumorHumansImmune Checkpoint InhibitorsMiceProgrammed Cell Death 1 ReceptorSuccinic AcidB7-H1 AntigenBezafibrateCarnitine O-PalmitoyltransferaseCD274 protein, humanCPT1A protein, humanImmune Checkpoint InhibitorsPDCD1 protein, humanProgrammed Cell Death 1 ReceptorSuccinic Acid

Identifiers

PMID40069506
PMCPMC11906371

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Registered trials

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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.