Evidence map›Paper›PMID 42290659›Full record

ArticleGenes & diseases2026

IRP1/ARID3A complex promotes pancreatic cancer chemoresistance by suppressing CYGB-related ferroptosis.

Zeru Li, Cheng Qin, Bangbo Zhao, Tianyu Li, Yutong Zhao, Lirui Huang, Haoyu Shi, Yiping Xie, Yutong Yan, Xiangyu Zhang and 1 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Genes & diseases, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

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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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

11 authors.

Zeru LiDepartment of General Surgery, State Key Laboratory of Complex Severe and Rare Diseases, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100730, China.
Cheng QinDepartment of General Surgery, State Key Laboratory of Complex Severe and Rare Diseases, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100730, China.
Bangbo ZhaoDepartment of General Surgery, State Key Laboratory of Complex Severe and Rare Diseases, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100730, China.
Tianyu LiDepartment of General Surgery, State Key Laboratory of Complex Severe and Rare Diseases, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100730, China.
Yutong ZhaoDepartment of General Surgery, State Key Laboratory of Complex Severe and Rare Diseases, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100730, China.
Lirui HuangDepartment of General Surgery, State Key Laboratory of Complex Severe and Rare Diseases, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100730, China.
Haoyu ShiDepartment of General Surgery, State Key Laboratory of Complex Severe and Rare Diseases, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100730, China.
Yiping XieDepartment of General Surgery, State Key Laboratory of Complex Severe and Rare Diseases, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100730, China.
Yutong YanDepartment of General Surgery, State Key Laboratory of Complex Severe and Rare Diseases, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100730, China.
Xiangyu ZhangDepartment of General Surgery, State Key Laboratory of Complex Severe and Rare Diseases, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100730, China.
Weibin WangDepartment of General Surgery, State Key Laboratory of Complex Severe and Rare Diseases, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100730, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ferroptosis, a unique modality of regulated cell death, has become an emerging strategy for tumor therapy. Multiple cellular pathways, including redox homeostasis, iron handling, epigenetic regulation, and metabolic changes, could mediate ferroptosis. Here, we demonstrate that high expression of iron-responsive element binding protein (IRP1)/A + T rich interaction domain protein 3a (ARID3A) inhibits ferroptosis and enhances chemoresistance of pancreatic cancer cells via handling the promoter region of a ferroptosis gene, cytoglobin (CYGB). Mechanistically, the high level of iron leads to nuclear translocation of IRP1 and ARID3A, thereby mediating ARID3A binding to the promoter region of CYGB and down-regulation of chromatin accessibility. The decrease of CYGB expression results in pancreatic cancer cell resistance to ferroptosis, which makes them more resistant to chemotherapy. Clinically, high expression of IRP1 and ARID3A associates with unsatisfactory chemotherapeutic response and poor survival of patients with pancreatic cancer. Our study highlights the role of IRP1/ARID3A complex as a chemotherapy target and its potential in the combined application of ferroptosis drugs.

Indexed as

ChemosensitivityChromatin accessibilityEpigeneticsFerroptosisPancreatic cancer

Identifiers

PMID42290659
PMCPMC13254595

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.