Evidence map›Paper›PMID 41663394›Full record

ArticleNature communications2026

Histone lactylation increases CXCL1 expression for neutrophil infiltration and immune escape in pancreatic cancer.

Peng Zhang, Jinrong Ma, Yi Wan, Chenxi Li, Lijuan Liu, Mengmeng He, Ning Zhang, Yanfen Ma, Jian Hu, Liyuan Zhao and 11 more

Abstract read
In one paragraph

Article in Nature communications, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing 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

7 citing papers in PubMed.

  1. Leveraging Microphysiological Systems to Facilitate Neutrophil-Based Cancer Immunotherapy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
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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

21 authors.

Peng Zhang *Center for Molecular Diagnosis and Precision Medicine, The First Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, China.
Jinrong Ma *Center for Molecular Diagnosis and Precision Medicine, The First Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, China.
Yi Wan *Center for Molecular Diagnosis and Precision Medicine, The First Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, China.
Chenxi Li *Center for Molecular Diagnosis and Precision Medicine, The First Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, China.ORCID 0009-0008-6029-7180
Lijuan Liu *Precision Medicine center, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China.
Mengmeng HeCenter for Molecular Diagnosis and Precision Medicine, The First Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, China.
Ning ZhangDepartment of Clinical Laboratory, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China.
Yanfen MaDepartment of Clinical Laboratory, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China.
Jian HuDepartment of Clinical Laboratory, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China.
Liyuan ZhaoCenter for Molecular Diagnosis and Precision Medicine, The First Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, China.ORCID 0009-0006-2586-582X
Ziwei ZhongCenter for Molecular Diagnosis and Precision Medicine, The First Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, China.
Xiao LeiCenter for Molecular Diagnosis and Precision Medicine, The First Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, China.
Jin GongCancer Center, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China.
Ting ZengCenter for Molecular Diagnosis and Precision Medicine, The First Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, China.
Junpeng MaCenter for Molecular Diagnosis and Precision Medicine, The First Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, China.
Yanyan DaCenter for Molecular Diagnosis and Precision Medicine, The First Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, China.
Zhiyong ZhouCenter for Molecular Diagnosis and Precision Medicine, The First Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, China.
Jin YangCancer Center, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China.
Xiaoqin WangDepartment of Clinical Laboratory, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China.
Tian GongCenter for Molecular Diagnosis and Precision Medicine, The First Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, China.
Chengsheng ZhangCenter for Molecular Diagnosis and Precision Medicine, The First Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, China. cszhang99@ncu.edu.cn.ORCID 0000-0002-5238-083X

Funding

National Natural Science Foundation of China (National Science Foundation of China) 32200639Natural Science Foundation of Jiangxi Province (Jiangxi Province Natural Science Foundation) 20224BAB216066
6 · The paper itself

Abstract

Aerobic glycolysis and lactate have been shown to modulate tumor microenvironment (TME) and disease progression. Lactate-mediated histone lysine lactylation (Kla) is a newly recognized epigenetic modification whose biological function remains poorly understood. Here, through integrated bioinformatic and experimental analyses, we demonstrate that glycolysis-derived lactate induces histone H3 lysine 18 lactylation (H3K18la) and up-regulates the expression of chemokine C-X-C motif Ligand 1 (CXCL1), thereby recruiting neutrophils and inducing immunosuppression in pancreatic cancer. Moreover, our data suggest that p300/CBP-associated factor (PCAF) functions as a histone lactyltransferase that transcriptionally activates CXCL1 expression. Finally, we reveal that combinational treatment with bromosporine (a PCAF inhibitor) and anti-PD-1 antibody exhibits a synergistic antitumor effect on both subcutaneous and orthotopic tumor models of pancreatic cancer. Taken together, our study not only identifies a mechanism by which the aerobic glycolysis-induced Lactate-PCAF-H3K18la-CXCL1 pathway mediates neutrophil infiltration and immunosuppression, but also develops a potential therapeutic strategy for pancreatic cancer.

Indexed as

Chemokine CXCL1HistonesNeutrophil InfiltrationPancreatic NeoplasmsTumor EscapeAnimalsCell Line, TumorFemaleGene Expression Regulation, NeoplasticGlycolysisHumansLactic AcidMiceNeutrophilsp300-CBP-Associated Factorp300-CBP Transcription FactorsChemokine CXCL1CXCL1 protein, humanHistonesLactic Acidp300-CBP-Associated Factorp300-CBP Transcription Factors

Identifiers

PMID41663394
PMCPMC12996564

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.