ArticleCancer cell international2022
E2F6/KDM5C promotes SF3A3 expression and bladder cancer progression through a specific hypomethylated DNA promoter.
Article in Cancer cell international, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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15 citing papers in PubMed, 15 citations in OpenAlex.
- LRRFIP1 Inhibits White Adipocyte Differentiation by Suppressing the E2F6/C/EBPα Axis.Diabetes & metabolism journal · 2026Article
- Transcription Factor MAX Regulates Liver Cancer Cell Growth, Migration, Invasion, and Epithelial-Mesenchymal Transition by Promoting SF3A3 Expression.World journal of oncology · 2026Article
- Article
- Noncanonical role of KDM5C in conferring bortezomib resistance via the PERK‒Nrf2 axis in multiple myeloma.Cell death & disease · 2026Article
- ERRα-KDM5C restrains STING enhancer activity to modulate type I interferon signaling in breast cancer progression.Cell death & disease · 2026Article
- Mechanism of KDM5C-Mediated H3K4me3 Demethylation of HOXC-AS3 in the Proliferation of Colorectal Cancer Cells.The Kaohsiung journal of medical sciences · 2025Article
- SF3A3 Drives Tumorigenesis in Endometrial Cancer by Enhancing c-FOS Expression and Represents a Potential Therapeutic Target.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Trans-ancestry transcriptome-wide association and functional studies to uncover novel susceptibility genes and therapeutic targets for colorectal cancer.NPJ precision oncology · 2025Article
- Interaction of STIL with FOXM1 regulates SF3A3 transcription in the hepatocellular carcinoma development.Cell division · 2025Article
- Article
- Review
- Discovery and structural studies of histone demethylases.Frontiers in epigenetics and epigenomics · 2025Review
- Alternative splicing regulation and its therapeutic potential in bladder cancer.Frontiers in oncology · 2024Review
- Tumor-associated macrophage-derived exosomes LINC01592 induce the immune escape of esophageal cancer by decreasing MHC-I surface expression.Journal of experimental & clinical cancer research : CR · 2023Article
- Transcriptome Analysis in Patients With Muscle-invasive Bladder Cancer.In vivo (Athens, Greece)Article
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10 authors at 1 institution in 1 country.
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Abstract
backgroundAbnormal expression of splicing factor 3A subunit 3 (SF3A3), a component of the spliceosome, has been confirmed to be related to the occurrence and development of various cancers. However, the expression and function of SF3A3 in bladder cancer (BC) remains unclear.
methodsThe SF3A3 mRNA and protein level were measured in clinical samples and cell lines by quantitative real-time PCR, Western blot and immunofluorescence staining. Evaluate the clinical correlation between SF3A3 expression and clinicopathological characteristics through statistical analysis in BC patients. The function of SF3A3 in BC cells was determined in vitro using MTT and colony analysis. Co-immunoprecipitation (CoIP) assay was used to detected E2F6 and KDM5C interaction. Luciferase reporter and chromatin immunoprecipitation (ChIP) were used to examine the relationship between E2F6/KDM5C and SF3A3 expression.
resultsIn the present study, we demonstrated that expression of SF3A3 was elevated in BC tissue compared to the normal bladder tissue. Importantly, the upregulation of SF3A3 in patients was correlated with poor prognosis. Additionally, overexpression of SF3A3 promoted while depletion of SF3A3 reduced the growth of BC cells in vivo and in vitro. Data from the TCGA database and clinical samples revealed that hypomethylation of the DNA promoter leads to high expression of SF3A3 in BC tissue. We found that upregulation of lysine-specific demethylase 5C (KDM5C) promotes SF3A3 expression via hypomethylation of the DNA promoter. The transcription factor E2F6 interacts with KDM5C, recruits KDM5C to the SF3A3 promoter, and demethylates the GpC island of H3K4me2, leading to high SF3A3 expression and BC progression.
conclusionsThe results demonstrated that depletion of the KDM5C/SF3A3 prevents the growth of BC in vivo and in vitro. The E2F6/KDM5C/SF3A3 pathway may be a potential therapeutic target for BC treatment.
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