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ARID1A has prognostic value in acute myeloid leukemia and promotes cell proliferation via TGF-β1/SMAD3 signaling.

Authors
  • Ren, Tianying1
  • Wang, Jing2
  • Tang, Wenqiang3
  • Chen, Dongliang1
  • Wang, Shuang1
  • Zhang, Xiaole4
  • Yang, Dawei5
  • 1 Zhong Yuan Academy of Biological Medicine, Liaocheng People's Hospital, Liaocheng, 252000, Shandong, People's Republic of China. , (China)
  • 2 Key Laboratory for Pediatrics of Integrated Traditional and Western Medicine, Liaocheng People's Hospital, Liaocheng, 252000, Shandong, People's Republic of China. , (China)
  • 3 Central Laboratory, Liaocheng People's Hospital, Liaocheng, 252000, Shandong, People's Republic of China. , (China)
  • 4 Department of Hematology, Liaocheng People's Hospital, Liaocheng, 252000, Shandong, People's Republic of China. [email protected]. , (China)
  • 5 Zhong Yuan Academy of Biological Medicine, Liaocheng People's Hospital, Liaocheng, 252000, Shandong, People's Republic of China. [email protected]. , (China)
Type
Published Article
Journal
Clinical and experimental medicine
Publication Date
Jul 01, 2023
Volume
23
Issue
3
Pages
777–785
Identifiers
DOI: 10.1007/s10238-022-00863-8
PMID: 35867200
Source
Medline
Keywords
Language
English
License
Unknown

Abstract

Previous studies have shown that the gene AT-rich interactive domain-containing protein 1A (ARID1A) is a subunit of SWI/SNF chromatin remodeling complex that acts as a tumor suppressor gene in several cancers and plays a vital role in tumorigenesis. However, its biological functions in acute myeloid leukemia (AML) are still unclear. Here, we tried to elaborate the expression of ARID1A in patients with AML, in leukemia cells, as well as the molecular mechanisms. Our results indicated that the expression of ARID1A was significantly downregulated in the bone marrow of patients with AML and relapsed patients compared with healthy subjects and patients in complete remission. Meantime, receiver operating characteristic curve analysis showed that the expression of ARID1A could be used to discriminate between patients with AML and patients in complete remission. We further constructed a knockdown cell model to determine the regulatory mechanisms of ARID1A in AML cells. We found that the decreased expression of ARID1A promoted cell proliferation, suppressed cellular apoptosis, and impeded cell cycle arrest via TGF-β1/SMAD3 signaling pathway. These results revealed that the reduced expression of ARID1A promoted cell proliferation via the TGF-β1/SMAD3 cascade and served as a prognostic biomarker for AML and therapeutic targets. © 2022. The Author(s), under exclusive licence to Springer Nature Switzerland AG.

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