Evidence map›Paper›PMID 39034411›Full record

ArticleJournal of experimental & clinical cancer research : CR2024

CXCL5 impedes CD8

Dantong Sun, Lipin Tan, Yongbing Chen, Qiang Yuan, Kanqiu Jiang, Yangyang Liu, Yuhang Xue, Jinzhi Zhang, Xianbao Cao, Minzhao Xu and 5 more

Abstract read
In one paragraph

Article in Journal of experimental & clinical cancer research : CR, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing 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

30 citing papers in PubMed.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Review
  6. Review
  7. Progress in Designing Cytokine Antagonist Antibodies for Cancer Therapy.BioDrugs : clinical immunotherapeutics, biopharmaceuticals and gene therapy · 2026
    Review
  8. Review
  9. Article
  10. Review
  11. Article
  12. Review
  13. Article
  14. Review
  15. PD-L1Frontiers in immunology · 2026
    Article
  16. Article
  17. Article
  18. Article
  19. Review
  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

15 authors.

Dantong Sun *Department of Thoracic and Cardiac Surgery, The Second Affiliated Hospital of Soochow University, Suzhou, 215004, China.
Lipin Tan *Department of nursing administration, The Second Affiliated Hospital of Soochow University, Suzhou, 215004, China.
Yongbing Chen *Department of Thoracic and Cardiac Surgery, The Second Affiliated Hospital of Soochow University, Suzhou, 215004, China.
Qiang Yuan *Department of interventional medicine, The Second Affiliated Hospital of Soochow University, Suzhou, 215004, China.
Kanqiu JiangDepartment of Thoracic and Cardiac Surgery, The Second Affiliated Hospital of Soochow University, Suzhou, 215004, China.
Yangyang LiuDepartment of Vascular Surgery, Hospital of Zhangjiagang, Suzhou, 215600, China.
Yuhang XueDepartment of Thoracic Surgery, Hospital of Yancheng, Yancheng, 224000, China.
Jinzhi ZhangDepartment of Thoracic and Cardiac Surgery, The Second Affiliated Hospital of Soochow University, Suzhou, 215004, China.
Xianbao CaoDepartment of Thoracic and Cardiac Surgery, The Second Affiliated Hospital of Soochow University, Suzhou, 215004, China.
Minzhao XuDepartment of Thoracic and Cardiac Surgery, The Second Affiliated Hospital of Soochow University, Suzhou, 215004, China.
Yang LuoDepartment of Thoracic and Cardiac Surgery, The Second Affiliated Hospital of Soochow University, Suzhou, 215004, China.
Zhonghua XuDepartment of Thoracic and Cardiac Surgery, The Second Affiliated Hospital of Soochow University, Suzhou, 215004, China.
Zhonghen XuDepartment of Thoracic and Cardiac Surgery, The Second Affiliated Hospital of Soochow University, Suzhou, 215004, China.
Weihua XuDepartment of Thoracic and Cardiac Surgery, The Second Affiliated Hospital of Soochow University, Suzhou, 215004, China.
Mingjing ShenDepartment of Thoracic and Cardiac Surgery, The Second Affiliated Hospital of Soochow University, Suzhou, 215004, China. shenmingjing0707@126.com.ORCID http://orcid.org/0000-0002-7918-0803

Funding

Gusu Health Talent Program of Suzhou GSWS2021020, GSWS2023045 and GSWS2022147Hospital Internal Research Foundation SDFEYBS2009, SDFEYJGL2101 and SDFEYHL2255Jiangsu Key Research and Social Development Projec BE2020653Key Scientific Program of Jiangsu Provincial Health Commission ZD2021033National Key Laboratory of Neural and Tumorous Drug Development SIML202301National Key Laboratory of Radiation Medicine and Auxiliary Protection GZK12023032National Natural Science Foundation of China 82172076Project of Medical New Technology Assistance of the Second Affiliated Hospital of Soochow University 23ZL004 and 23ZL012Science and Technology Program of Suzhou SKJY2021077, SKY2022166, and SKYD2023117the Technological Innovation Project of CNNC Medical Industry Co. Ltd ZHYLYB2021007
6 · The paper itself

Abstract

backgroundLung cancer remains one of the most prevalent cancer types worldwide, with a high mortality rate. Upregulation of programmed cell death protein 1 (PD-1) and its ligand (PD-L1) may represent a key mechanism for evading immune surveillance. Immune checkpoint blockade (ICB) antibodies against PD-1 or PD-L1 are therefore widely used to treat patients with lung cancer. However, the mechanisms by which lung cancer and neutrophils in the microenvironment sustain PD-L1 expression and impart stronger inhibition of CD8

methodsWe investigated the role and underlying mechanism by which PD-L1

resultsWe demonstrated that C-X-C motif chemokine ligand 5 (CXCL5) is markedly overexpressed in lung cancer cells and is positively correlated with a poor prognosis in patients with lung cancer. Mechanistically, CXCL5 activates the phosphorylation of the Paxillin/AKT signaling cascade, leading to upregulation of PD-L1 expression and the formation of a positive feedback loop. Moreover, CXCL5 attracts neutrophils, compromising CD8

conclusionsOur findings collectively demonstrate that CXCL5 promotes immune escape through PD-L1 upregulation in lung cancer and neutrophils chemotaxis through autocrine and paracrine mechanisms. CXCL5 may serve as a potential therapeutic target in synergy with ICBs in lung cancer immunotherapy.

Indexed as

B7-H1 AntigenCD8-Positive T-LymphocytesChemokine CXCL5Lung NeoplasmsNeutrophilsProto-Oncogene Proteins c-aktAnimalsChemotaxisFemaleHumansMaleMiceMice, Inbred NODMice, SCIDPhosphorylationSignal TransductionB7-H1 AntigenCD274 protein, humanChemokine CXCL5CXCL5 protein, humanProto-Oncogene Proteins c-aktCXCL5NeutrophilsPD-L1PXN/AKT signalingT cell immunity

Identifiers

PMID39034411
PMCPMC11264977

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