Evidence mapPaperPMID 39922804Full record

ArticleCell death discovery2025

Anaerobic metabolism promotes breast cancer survival via Histone-3 Lysine-18 lactylation mediating PPARD axis.

Ying Xu, Weiwei Meng, Yingqi Dai, Lin Xu, Ning Ding, Jinqing Zhang, Xuewei Zhuang

Abstract read
In one paragraph

Article in Cell death discovery, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing 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

23 citing papers in PubMed.

  1. Unveiling Lactylation: A Novel Frontier in Cancer Stemness and Therapy.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

7 authors.

Ying Xu *Department of Thyroid and Breast Surgery, Shandong Provincial Third Hospital, Shandong University, Jinan, China. xuying2205@126.com.ORCID http://orcid.org/0000-0002-8941-7560
Weiwei MengDepartment of Clinical Laboratory, Shandong Provincial Third Hospital, Shandong University, Jinan, China.
Yingqi DaiDepartment of Thyroid and Breast Surgery, Shandong Provincial Third Hospital, Shandong University, Jinan, China.
Lin XuTranslational Medicine Laboratory, Shandong Provincial Third Hospital, Shandong University, Jinan, China.
Ning DingDepartment of Anesthesiology, Shandong Provincial Key Medical and Health Laboratory of Intensive Care Rehabilitation, Shandong Provincial Third Hospital, Cheeloo College of Medicine, Shandong University, Jinan, China.
Jinqing Zhang *Department of Thyroid and Breast Surgery, Shandong Provincial Third Hospital, Shandong University, Jinan, China. 95190687@qq.com.
Xuewei Zhuang *Department of Clinical Laboratory, Shandong Provincial Third Hospital, Shandong University, Jinan, China. zhuangxuewei@sdu.edu.cn.

Funding

Natural Science Foundation of Shandong Province (Shandong Provincial Natural Science Foundation) ZR2020MH321
6 · The paper itself

Abstract

Histone lactylation plays a crucial role in cancer progression, but its impact on breast cancer (BC) tumorigenesis is still unclear. We utilized chromatin immunoprecipitation sequencing with H3K18la antibodies, transcriptomics of clinical BC samples, and proteomics and ATAC-seq analyses of in vivo tumors to identify the genes regulated by H3K18la and the transcription factor PPARD. qPCR and Western blot assays were used to detect expressions of molecules. We discovered that H3K18la levels were higher in BC tissues compared to adjacent non-cancerous tissues. H3K18la promoted the expression of PPARD, which in turn influenced the transcription of AKT, but not ILK. ATAC-seq analysis revealed that glycolysis in BC cells enhanced chromatin accessibility. Additionally, we confirmed that HDAC2 and HDAC3 act as "erasers" for H3 lysine lactylation. During the proteomics analysis, AKT-phosphorylation in the aerobic respiration inhibitor group exhibited an apparent disparity and activity. Our study demonstrated that changes in H3K18la in BC and its downstream transcription factor PPARD support cell survival under anaerobic glycolysis conditions. PPARD accelerated cancer proliferation by promoting the transcription and phosphorylation of AKT. This highlights the therapeutic potential of targeting the H3K18la/PPARD/AKT axis in breast cancer, providing new insights into epigenetic regulation and cancer metabolism (Trial registration: The study was approved by the Research Ethics Committee Shandong Provincial Third Hospital (KYLL-2023057; https://www.medicalresearch.org.cn/ )).

Identifiers

PMID39922804
PMCPMC11807217

What Socratic holds

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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 Socratic graph.