Chromatin Remodeling-Related PRDM1 Increases Stomach Cancer Proliferation and Is Counteracted by Bromodomain Inhibitor

Sep 21, 2026

Gastrointestinal (GI) cancers pose major public health threats, and existing surgery, chemotherapy, and targeted therapy achieve limited mortality reduction, requiring additional therapeutic targets. Systematic bioinformatic analysis across 31 chromatin remodeling factors in six GI cancers identified PRDM1 as showing both expression changes and prognostic value. Pathway and mediator analyses linked PRDM1-high stomach cancer to cell-cycle signaling and BET/bromodomain inhibition via IBET151 and BRD4, supported by cell-line experiments in SNU-1.

LanguageEnglish

CategoryResearch & Report

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Pages22

Reading Time55 min

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1. Introduction

Chromatin remodeling and GI cancer context

Epigenetic therapeutics and therapeutic target need

Article Chromatin Remodeling-Related PRDM1 Increases Stomach Cancer Proliferation and Is Counteracted by Bromodomain Inhibitor Yu-Hsuan Hung 1, *,†, Hui-Ching Wang 2,†, Mei-Ren Pan 3 and Li-Tzong Chen 4,5,6,7, * Citation: Hung, Y.-H.; Wang, H.-C.; Pan, M.-R.; Chen, L.-T. Chromatin Remodeling-Related PRDM1 Increases Stomach Cancer Proliferation and Is Counteracted by Bromodomain Inhibitor. J. Pers. Med. 2024, 14, 224. [https://doi.org/](https://doi.org/)[ ](https://doi.org/)[10.3390/jpm14030224](10.3390/jpm14030224) Academic Editor: Maximos Frountzas Received: 11 January 2024 Revised: 7 February 2024 Accepted: 18 February 2024 Published: 20 February 2024 Copyright: © 2024 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ([https://](https://)[ ](https://)[creativecommons.org/licenses/by/](creativecommons.org/licenses/by/)[ ](creativecommons.org/licenses/by/)[4.0/](4.0/)) . 1 Department of Medical Research, Kaohsiung Medical University Hospital, Kaohsiung Medical University, Kaohsiung 807, Taiwan 2 Division of Hematology and Oncology, Department of Internal Medicine, Kaohsiung Medical University Hospital, Kaohsiung Medical University, Kaohsiung 807, Taiwan; [joellewang66@gmail.com](joellewang66@gmail.com) 3 Graduate Institute of Clinical Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung 807, Taiwan; [mrpan@cc.kmu.edu.tw](mrpan@cc.kmu.edu.tw) 4 Drug Development and Value Creation Research Center, Kaohsiung Medical University, Kaohsiung 807, Taiwan 5 National Institute of Cancer Research, National Health Research Institutes, Tainan 704, Taiwan 6 Division of Gastroenterology, Department of Internal Medicine, Kaohsiung Medical University Hospital, Kaohsiung Medical University, Kaohsiung 807, Taiwan 7 Center for Cancer Research, Kaohsiung Medical University, Kaohsiung 807, Taiwan * [Correspondence: yhhung2021@gmail.com](Correspondence: yhhung2021@gmail.com) (Y.-H.H.); [leochenk153@gmail.com](leochenk153@gmail.com) (L.-T.C.)† These authors contributed equally to this work. Abstract: Gastrointestinal (GI) cancers are some of the main public health threats to the world. Even though surgery, chemotherapy, and targeted therapy are available for their treatments, these approaches provide limited success in reducing mortality, making the identification of additional therapeutic targets mandatory. Chromatin remodeling in cancer has long been studied and related therapeutics are widely used, although less is known about factors with prognostic and therapeutic potential in such areas as gastrointestinal cancers. Through applying systematic bioinformatic analysis, we determined that out of 31 chromatin remodeling factors in six gastrointestinal cancers, only PR/SET domain 1 (PRDM1) showed both expression alteration and prognosis prediction. Analyses on pathways, therapies, and mediators showed that cell cycle, bromodomain inhibitor IBET151, and BET protein BRD4 were, respectively involved in PRDM1-high stomach cancer, while cell line experiments validated that PRDM1 knockdown in human stomach cancer cell line SNU-1 decreased its proliferation, BRD4 expression, and responsiveness to IBET151; accordingly, these results indicate the contribution by PRDM1 in stomach cancer formation and its association with BRD4 modulation as well as BET inhibitor treatment. Keywords: PRDM1; stomach cancer; BET inhibitor; BRD4 1. Introduction Gastrointestinal (GI) cancers are some of the most menacing diseases globally [1,2], containing tumors that originate from the head and neck, stomach, liver, bile duct, pancreas, and colon [1,2]. In the US, cancers originating from the colon and pancreas rank 3rd and 4th in both sexes [3]; liver cancer ranks 5th in males and 7th in females; while head and neck cancers rank 7th in males. In Taiwan, cancers originating from the liver,

FAQs

What problem does the article address in GI cancer treatment?

It addresses limited success of current therapies in reducing mortality, motivating the search for additional therapeutic targets.

How was PRDM1 identified as relevant to GI cancers?

By systematic bioinformatic analysis of 31 chromatin remodeling factors across six GI cancers, where PRDM1 showed both expression alteration and prognosis prediction.

What experimental evidence supports PRDM1’s role in stomach cancer?

Cell line experiments showed that PRDM1 knockdown in the SNU-1 stomach cancer line decreased proliferation and reduced BRD4 expression, and affected responsiveness to IBET151.

Sep 21, 2026

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