Evidence map›Paper›PMID 41605861›Full record

ArticleJournal of cellular and molecular medicine2026

ARID3A Dysregulation Drives Colon Cancer Progression and Enhances Responsiveness to Aspirin.

Jiade Li, Muhan Li, Quanfu Li, Yungaowa Wu, Yifan Shen, Yanping Li, Mingshuo Zhang, Guangyou Wang, Yuanyuan Zhu

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of cellular and molecular medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

9 authors.

Jiade LiDepartment of Neurobiology, School of Basic Medical, Harbin Medical University, Harbin, Heilongjiang, P.R. China.
Muhan LiDepartment of Pathology, School of Basic Medical, Harbin Medical University, Harbin, Heilongjiang, P.R. China.
Quanfu LiDepartment of Medical Oncology, Ordos Central Hospital, Ordos, Inner Mongolia, P.R. China.ORCID https://orcid.org/0000-0002-0309-3359
Yungaowa WuDepartment of Medical Oncology, Ordos Central Hospital, Ordos, Inner Mongolia, P.R. China.
Yifan ShenDepartment of Pathology, School of Basic Medical, Harbin Medical University, Harbin, Heilongjiang, P.R. China.
Yanping LiDepartment of Pathology, School of Basic Medical, Harbin Medical University, Harbin, Heilongjiang, P.R. China.
Mingshuo ZhangDepartment of Pathology, School of Basic Medical, Harbin Medical University, Harbin, Heilongjiang, P.R. China.
Guangyou WangDepartment of Neurobiology, School of Basic Medical, Harbin Medical University, Harbin, Heilongjiang, P.R. China.
Yuanyuan ZhuDepartment of Pathology, School of Basic Medical, Harbin Medical University, Harbin, Heilongjiang, P.R. China.

Funding

Natural Science Foundation of Heilongjiang Province LH2023H010Public Hospital Research Joint Fund Science and Technology Project 2024GLLH1311Science foundation of Haiyan JJQN2019-06the Open Project Program of Key Laboratory of Preservation of Human Genetic Resources and Disease Control in China (Harbin Medical University), Ministry of Education LPHGRD 2023-006
6 · The paper itself

Abstract

The AT-Rich Interaction Domain (ARID) family plays critical roles in malignancies. Although numerous members have been shown to influence cancer processes, there is a lack of a general understanding of the ARID family in colon cancer. To address this gap, we used bioinformatic technologies to investigate the role of the ARID family as a whole and to identify the crucial member. Subsequently, cell growth assays, transwell assays, and animal models were employed to validate the key member's effect on colon cancer growth and metastasis. Furthermore, bioinformatics and immunohistochemistry were utilised to explore the potential mechanisms and evaluate the efficacy of a targeted intervention strategy. Our results showed that the ARID family was upregulated in colon cancer, with ARID3A being the main component that promoted colon cancer development. Specifically, ARID3A enhanced colon cancer cell proliferation, migration, and invasion both in vivo and in vitro. Mechanistically, this promotional effect could be associated with ARID3A promoting PGE2 synthesis and triggering macrophage infiltration. Notably, aspirin treatment reduced the PGE2 level, which significantly inhibited the malignant behaviour of ARID3A-overexpressing cells. In conclusion, ARID3A was a key member of the ARID family in the development of colon cancer. ARID3A was an underlying biomarker for aspirin administration.

Indexed as

AspirinColonic NeoplasmsDNA-Binding ProteinsGene Expression Regulation, NeoplasticTranscription FactorsAnimalsCell Line, TumorCell MovementCell ProliferationDisease ProgressionHumansMiceXenograft Model Antitumor AssaysARID3A protein, humanAspirinDNA-Binding ProteinsTranscription FactorsARID3AARID familyaspirincolon cancermacrophage

Identifiers

PMID41605861
PMCPMC12851895

What OpenQuestion 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 OpenQuestion graph.