Evidence map›Paper›PMID 40234906›Full record

ArticleJournal of translational medicine2025

Cold atmospheric plasma drives USP49/HDAC3 axis mediated ferroptosis as a novel therapeutic strategy in endometrial cancer via reinforcing lactylation dependent p53 expression.

Jinlin Liu, Yang Li, Ruonan Ma, Youming Chen, Jinyang Wang, Lindong Zhang, Baojin Wang, Zidi Zhang, Lili Huang, Hongyan Zhang and 2 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of translational medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
14citing 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

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

  1. Pooled it
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  4. Lactate-Mediated Lysine Lactylation in Renal Fibrosis: Current Progress and Challenges.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 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

12 authors.

Jinlin Liu *Department of Obstetrics and Gynecology, The Third Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China.
Yang Li *Department of Clinical Laboratory, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China.
Ruonan MaHenan Key Laboratory of Ion-beam Bioengineering, Zhengzhou University, Zhengzhou, Henan, China.
Youming ChenDepartment of Clinical Laboratory, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China.
Jinyang WangHenan Key Laboratory of Ion-beam Bioengineering, Zhengzhou University, Zhengzhou, Henan, China.
Lindong ZhangDepartment of Obstetrics and Gynecology, The Third Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China.
Baojin WangDepartment of Obstetrics and Gynecology, The Third Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China.
Zidi ZhangDepartment of Obstetrics and Gynecology, The Third Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China.
Lili HuangDepartment of Obstetrics and Gynecology, Yongcheng Maternal and Child Health Hospital, Shangqiu, Henan, China.
Hongyan ZhangDepartment of Obstetrics and Gynecology, Yongcheng Maternal and Child Health Hospital, Shangqiu, Henan, China.
Junhu WanDepartment of Clinical Laboratory, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China. wanjh@zzu.edu.cn.ORCID 0009-0008-3869-7153
Hongyang LiuDepartment of Obstetrics and Gynecology, The Third Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China. lhy0980@zzu.edu.cn.

Funding

Henan Province Science and Technology Research and Development Joint Fund Grant No. 242301420071National Natural Science Foundation of China Grant No. 82173018Natural Science Foundation of Henan Province Grant No.232300421054, 232300421286the Funding for Scientific Research and Innovation Team of The First Affiliated Hospital of Zhengzhou University Grant No. QNCXTD2023005the Medical Science and Technology Provincial and Ministerial Co-construction Project of Henan province Grant No. SBGJ202403034The Research and Practice Project of Education and Teaching Reform of Zhengzhou University Grant No. 2022ZZUJG298the Young and Middle-aged Health Science and Technology Innovation Talents Project of Henan province Grant No. YXKC2021036
6 · The paper itself

Abstract

backgroundEndometrial cancer ranks among the most common gynecological cancers, with increasing rates of incidence and death. Cold atmospheric plasma (CAP) has become a promising novel therapeutic approach for cancer treatment. Nevertheless, the specific impact of CAP on endometrial cancer remains inadequately characterized.

objectivesThis study aimed to investigate the effect of CAP on the progression of endometrial cancer and reveal its specific regulatory mechanisms.

methodsColony formation, EdU, wound-healing, and transwell assay were used to detect the effect of CAP on endometrial cancer progression. Proteomics is employed to identify potential targets and signaling pathways through which CAP impacts endometrial cancer cells. MDA, lipid ROS, and JC-1 MMP assays were used to detect ferroptosis. Immunoprecipitation-mass spectrometry, co-immunoprecipitation, immunofluorescence co-localization, and molecular docking were used to analyze USP49 and HDAC3 interactions. The tumor xenografts model determined that CAP inhibits endometrial cancer growth in vivo.

resultsThis study observed a significant inhibitory effect of CAP on the proliferation and migration of endometrial cancer cells and reported for the first time that CAP induces ferroptosis in endometrial cancer cells. Mechanistically, CAP activated the transcription of p53 by modulating HDAC3 mediated the histone H3K18 lactylation, resulting in upregulation of p53 driving cell ferroptosis. The interaction between USP49 and HDAC3 was validated through mass spectrometry and co-immunoprecipitation experiments. The regulation of HDAC3 by CAP is contingent upon USP49, wherein the down-regulation of USP49 augments the ubiquitination of HDAC3, consequently diminishing its protein stability. Furthermore, animal models with transplanted tumors corroborated the inhibitory impact of CAP on endometrial cancer in vivo.

conclusionsOur findings illustrate the suppressive effect of CAP treatment on endometrial cancer and uncover a novel regulatory mechanism mediated by CAP. Specifically, CAP modulates the ferroptosis pathway through the HDAC3/H3K18la/p53 axis, presenting a novel therapeutic approach for endometrial cancer treatment.

Indexed as

Endometrial NeoplasmsFerroptosisHistone DeacetylasesPlasma GasesTumor Suppressor Protein p53Ubiquitin-Specific ProteasesAnimalsCell Line, TumorCell MovementCell ProliferationFemaleHistone Deacetylase 3HistonesHumansMiceMice, NudeHistone Deacetylase 3Histone DeacetylasesHistonesPlasma GasesTumor Suppressor Protein p53Ubiquitin-Specific ProteasesCAPEndometrial cancerFerroptosisHDAC3p53

Identifiers

PMID40234906
PMCPMC11998187

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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.