2. Academic Validation
  3. Chromatin Remodeling-Related PRDM1 Increases Stomach Cancer Proliferation and Is Counteracted by Bromodomain Inhibitor

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

  • J Pers Med. 2024 Feb 20;14(3):224. doi: 10.3390/jpm14030224.
Yu-Hsuan Hung 1,  Hui-Ching Wang 2,  Mei-Ren Pan 3,  Li-Tzong Chen 4 5 6 7
Affiliations

Affiliations

  • 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.
  • 3 Graduate Institute of Clinical Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung 807, Taiwan.
  • 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.
PMID: 38540967 DOI: 10.3390/jpm14030224
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

BET inhibitor; BRD4; PRDM1; stomach cancer.

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