ArticleCell death & disease2022
SF3B4 promotes ovarian cancer progression by regulating alternative splicing of RAD52.
Article in Cell death & disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 29 citations in OpenAlex.
- Switches in alternatively spliced isoforms impact protein and drug interactions in melanoma, ovarian cancer, and acute myeloid leukemia.British journal of cancer · 2026Article
- Expanded Polyglycine Protein Aggregates Alter the RNA Splicing Profile into a Premature State Partially via Sequestering SF3B4.Neuroscience bulletin · 2026Article
- The periphery of nuclear speckles defines a spatially and temporally regulated compartment of long-lived intron-retained RNAs that resolves during mitosis.Nature cell biology · 2026Article
- Pharmacological targeting of SF3a1-MDM4 splicing vulnerability in ovarian cancer with rifaximin and antisense oligonucleotide.Journal of translational medicine · 2026Article
- SF3B4 stabilizes SREBF1 via 3'UTR binding to drive hepatocellular carcinoma progression.Frontiers in oncology · 2026Article
- SNRPB-mediated regulation of DDX39A splicing promotes ovarian cancer progression by regulating α6 integrin subunit expression.Oncogene · 2025Article
- Pan-cancer oncogenic properties and therapeutic potential of SF3B4.Cancer gene therapy · 2025Article
- ALKBH5-mediated m6A regulates the alternative splicing events of SRSF10 in ovarian cancer.Cancer gene therapy · 2025Article
- ADCY5 Gene Affects Seasonal Reproduction in Dairy Goats by Regulating Ovarian Granulosa Cells Steroid Hormone Synthesis.International journal of molecular sciences · 2025Article
- Targeting the splicing factor SNRPB inhibits endometrial cancer progression by retaining the POLD1 intron.Experimental & molecular medicine · 2025Article
- Splicing factor 3b subunit 4 (SF3b4) is mediated by EP300 and CREBBP to promote colorectal cancer (CRC) proliferation by enhancing autophagy.American journal of cancer research · 2025Article
- Alternative splicing in ovarian cancer.Cell communication and signaling : CCS · 2024Review
- METTL3-mediated the m6A modification of SF3B4 facilitates the development of non-small cell lung cancer by enhancing LSM4 expression.Thoracic cancer · 2024Article
- SETDB1 promotes progression through upregulation of SF3B4 expression and regulates the immunity in ovarian cancer.Journal of ovarian research · 2024Article
- SF3B4 downregulation restrains lung adenocarcinoma tumorigenesis via 5' alternative splicing of KAT2A.Scientific reports · 2024Article
- Proteomics and Bioinformatics Investigations Link Overexpression of FGF8 and Associated Hub Genes to the Progression of Ovarian Cancer and Poor Prognosis.Biochemistry research international · 2024Article
- Circulating small extracellular vesicle-derived splicing factor 3b subunit 4 as a non-invasive diagnostic biomarker of early hepatocellular carcinoma.Journal of experimental & clinical cancer research : CR · 2023Article
- The role of alternative pre-mRNA splicing in cancer progression.Cancer cell international · 2023Review
- Parental mosaicism detection and preimplantation genetic testing in families with multiple transmissions of de novo mutations.Journal of medical genetics · 2023Article
- The splicing factor SNRPB promotes ovarian cancer progression through regulating aberrant exon skipping of POLA1 and BRCA2.Oncogene · 2023Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Many studies have proven that splicing factors are crucial for human malignant tumor development. However, as a classical splicing factor, the expression of SF3B4 is not clear, and its biological function needs to be further clarified in ovarian cancer (OC). We determined that SF3B4 was obviously upregulated and its high expression was associated with poor prognosis in OC patients. In vitro and in vivo assays suggested that SF3B4 overexpression promoted OC cell proliferation and mobility, and downregulation of SF3B4 had the opposite effect. Further studies found that miR-509-3p decreased SF3B4 mRNA expression by binding to the 3' -UTR of SF3B4 directly. Importantly, we revealed that RAD52 was a potential target of SF3B4 through alternative splicing events analysis. Loss of SF3B4 led to decreased expression of RAD52, owing to intron 8 retention and generation of premature termination codons. Moreover, decreased expression of RAD52 partially counteracted the tumor-promoting effect of SF3B4 overexpression. In conclusion, our results suggested that SF3B4, negatively regulated by miR-509-3p, promoted OC progression through effective splicing of RAD52. Therefore, SF3B4 may be a promising biomarker and effective therapeutic target for OC.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.