ArticleOncogene2021
SMARCA4 oncogenic potential via IRAK1 enhancer to activate Gankyrin and AKR1B10 in liver cancer.
Article in Oncogene, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 35 citations in OpenAlex.
- Gankyrin-Protein Interactions in GI Cancers: A Novel Target of New Therapeutics.Chronic diseases and translational medicine · 2025Review
- Dual tissue mRNA and serum protein signatures improve risk stratification in hepatocellular carcinoma.NPJ precision oncology · 2025Article
- ZDHHC12 Palmitoylates HDAC8 to Promote the Progression of Hepatocellular Carcinoma Associated with a Diet High in Saturated Fatty Acids.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- The role of SMARCA4 in lung cancer.Scientific reports · 2025Review
- Oncogenic function of growth arrest-specific transcript 5 by competing with miR-423-3p to regulate SMARCA4 in hepatocellular carcinoma.Experimental & molecular medicine · 2025Article
- Identification of key hub genes associated with anti-gastric cancer effects of lotus plumule based on machine learning algorithms.World journal of gastrointestinal oncology · 2025Article
- BRG1 promotes progression of B-cell acute lymphoblastic leukemia by disrupting PPP2R1A transcription.Cell death & disease · 2024Article
- Mammalian SWI/SNF complex activity regulates POU2F3 and constitutes a targetable dependency in small cell lung cancer.Cancer cell · 2024Article
- Preclinical evidence in the assembly of mammalian SWI/SNF complexes: Epigenetic insights and clinical perspectives in human lung disease therapy.Molecular therapy : the journal of the American Society of Gene Therapy · 2024Review
- SMARCA4‑deficient uterine adnexal tumor with ascites: A case report and literature review.Oncology letters · 2024Article
- Recent Advances in IRAK1: Pharmacological and Therapeutic Aspects.Molecules (Basel, Switzerland) · 2024Review
- Development of an orally bioavailable mSWI/SNF ATPase degrader and acquired mechanisms of resistance in prostate cancer.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Constructing a prognostic model for hepatocellular carcinoma based on bioinformatics analysis of inflammation-related genes.Frontiers in medicine · 2024Article
- AKR1B10 inhibits the proliferation and metastasis of hepatocellular carcinoma cells by regulating the PI3K/AKT pathway.Oncology letters · 2024Article
- Anticancer Effects of Wild Baicalin on Hepatocellular Carcinoma: Downregulation of AKR1B10 and PI3K/AKT Signaling Pathways.Cancer management and research · 2024Article
- Mammalian SWI/SNF chromatin remodeling complexes promote tyrosine kinase inhibitor resistance in EGFR-mutant lung cancer.Cancer cell · 2023Article
- BRG1: Promoter or Suppressor of Cancer? The Outcome of BRG1's Interaction with Specific Cellular Pathways.International journal of molecular sciences · 2023Review
- Bromodomain (BrD) Family Members as Regulators of Cancer Stemness-A Comprehensive Review.International journal of molecular sciences · 2023Review
- Delineation of a SMARCA4-specific competing endogenous RNA network and its function in hepatocellular carcinoma.World journal of clinical cases · 2022Article
- IRAK1 and IRAK4 as emerging therapeutic targets in hematologic malignancies.Current opinion in hematology · 2022Review
Corrections and comments
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Authors and funding
16 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
SWItch/Sucrose Non-Fermentable (SWI/SNF) is a multiprotein complex essential for the regulation of eukaryotic gene expression. SWI/SNF complex genes are genetically altered in over 20% of human malignancies, but the aberrant regulation of the SWI/SNF subunit genes and subsequent dysfunction caused by abnormal expression of subunit gene in cancer, remain poorly understood. Among the SWI/SNF subunit genes, SMARCA4, SMARCC1, and SMARCA2 were identified to be overexpressed in human hepatocellular carcinoma (HCC). Modulation of SMARCA4, SMARCC1, and SMARCA2 inhibited in vitro tumorigenesis of HCC cells. However, SMARCA4-targeting elicited remarkable inhibition in an in vivo Ras-transgenic mouse HCC model (Ras-Tg), and high expression levels of SMARCA4 significantly associated with poor prognosis in HCC patients. Furthermore, most HCC patients (72-86%) showed SMARCA4 overexpression compared to healthy controls. To identify SMARCA4-specific active enhancers, mapping, and analysis of chromatin state in liver cancer cells were performed. Integrative analysis of SMARCA4-regulated genes and active chromatin enhancers suggested 37 genes that are strongly activated by SMARCA4 in HCC. Through chromatin immunoprecipitation-qPCR and luciferase assays, we demonstrated that SMARCA4 activates Interleukin-1 receptor-associated kinase 1 (IRAK1) expression through IRAK1 active enhancer in HCC. We then showed that transcriptional activation of IRAK1 induces oncoprotein Gankyrin and aldo-keto reductase family 1 member B10 (AKR1B10) in HCC. The regulatory mechanism of the SMARCA4-IRAK1-Gankyrin, AKR1B10 axis was further demonstrated in HCC cells and in vivo Ras-Tg mice. Our results suggest that aberrant overexpression of SMARCA4 causes SWI/SNF to promote IRAK1 enhancer to activate oncoprotein Gankyrin and AKR1B10, thereby contributing to hepatocarcinogenesis.
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