Evidence map›Paper›PMID 41019373›Full record

ArticleiScience2025

Epigenetic-mediated positive feedback loop facilitates the progression of lung adenocarcinoma.

Yihang Cheng, Yifeng Luo, Tingting Hu, Qiaoling Ren, Li Xu, Tuo Yi, Yuan Tan, Wei Li, Xuxin Wang, Yaoxiang Sun and 7 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in iScience, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
  2. 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

17 authors.

Yihang ChengDepartment of Cardiology of The Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou 310009, China.
Yifeng LuoDepartment of Radiology, the Affiliated Yixing Hospital of Jiangsu University, Yixing 214200, China.
Tingting HuDepartment of Cardiology of The Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou 310009, China.
Qiaoling RenState Key Laboratory of Transvascular Implantation Devices, Zhejiang University, Hangzhou 310009, China.
Li XuDepartment of Cardiology of The Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou 310009, China.
Tuo YiDepartment of research and development, Zhejiang Gaomei Genomics, Hangzhou 310009, China.
Yuan TanKey Laboratory of Biological Targeting Diagnosis, Therapy and Rehabilitation of Guangdong Higher Education Institutes, The Fifth Affiliated Hospital of Guangzhou Medical University, Guangzhou 510300, China.
Wei LiKey Laboratory of Biological Targeting Diagnosis, Therapy and Rehabilitation of Guangdong Higher Education Institutes, The Fifth Affiliated Hospital of Guangzhou Medical University, Guangzhou 510300, China.
Xuxin WangDepartment of Pathology, the Affiliated Yixing Hospital of Jiangsu University, Yixing 214200, China.
Yaoxiang SunDepartment of Clinical Laboratory, the Affiliated Yixing Hospital of Jiangsu University, Yixing 214200, China.
Mingzhi ChenDepartment of Thoracic and Cardiovascular Surgery, the Affiliated Yixing Hospital of Jiangsu University, Yixing 214200, China.
Zhonghua ShenDepartment of Cardiovascular Surgery of The Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou 310009, China.
Bin ZhangState Key Laboratory of Transvascular Implantation Devices, Zhejiang University, Hangzhou 310009, China.
Youhuang BaiDepartment of Cardiology of The Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou 310009, China.
Yue TaoDepartment of research and development, Zhejiang Gaomei Genomics, Hangzhou 310009, China.
Zhihong CaoDepartment of Radiology, the Affiliated Yixing Hospital of Jiangsu University, Yixing 214200, China.
Deqiang SunDepartment of Cardiology of The Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou 310009, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Lung adenocarcinoma (LUAD) remains a leading cause of cancer-related mortality. We performed multi-omics approaches on LUAD samples spanning different stages, establishing a detailed epigenetic landscape. We identified 1,416 regions characterized by hypo-DNA methylation and hyperchromatin accessibility associated with high mortality and recurrence rates, serving as a biomarker panel for LUAD staging and diagnosis (AUC of 0.89 and 0.87 for two-class and multi-class models). Epigenetics-related transcription factors, especially the AP-1 family, were observed at these loci, and transcriptomic profiling indicated persistent activation of the mitogen-activated protein kinase (MAPK) signaling pathway. Hypomethylation and hyperaccessibility of AP-1 binding sites enhance EGFR and FGFBP1 expression, activating the MAPK pathway. This reveals an epigenetic-mediated positive feedback loop, MAPK→AP-1/Epigenetic Modifications→EGFR/FGFBP1→MAPK, in LUAD, highlighting the complex interplay between epigenetic modifications and LUAD progression, offering potential detection and treatment targets. These findings define a high-resolution, multi-stage epigenetic landscape of LUAD, providing a resource for biomarker discovery and mechanistic insight.

Indexed as

Biological sciencesMolecular biologyMolecular mechanism of gene regulation

Identifiers

PMID41019373
PMCPMC12475578

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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.