ArticleRNA (New York, N.Y.)2014
Elevated SRPK1 lessens apoptosis in breast cancer cells through RBM4-regulated splicing events.
Article in RNA (New York, N.Y.), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers, 2 of them syntheses that pooled it.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
50 citing papers in PubMed, 2 syntheses or guidelines pooled it, 82 citations in OpenAlex.
- Serine-Arginine Protein Kinase 1 (SRPK1): a systematic review of its multimodal role in oncogenesis.Molecular and cellular biochemistry · 2022Pooled it
- Alternative splicing and cancer: a systematic review.Signal transduction and targeted therapy · 2021Pooled it
- The translation landscape of ovarian clear cell carcinoma indicates that RBM4 plays a pro-oncogenic role in tumor progression.Oncogene · 2026Article
- Review
- A novel lncRNA-mediated signaling axis governs cancer stemness and splicing reprogramming in hepatocellular carcinoma with therapeutic potential.Journal of experimental & clinical cancer research : CR · 2025Article
- Epitranscriptomic sculpting: the role of mMedical oncology (Northwood, London, England) · 2025Review
- Best evidence linking the extracellular factor TGF-β to cancer-associated alternative splicing programs.BBA advances · 2025Review
- Tipping the balance of cell death: alternative splicing as a source of MCL-1S in cancer.Cell death & disease · 2024Review
- Identification and validation of protein biomarkers for predicting gastrointestinal stromal tumor recurrence.Computational and structural biotechnology journal · 2024Article
- SRPKs: a promising therapeutic target in cancer.Clinical and experimental medicine · 2023Review
- Chromosome-level Asian elephant genome assembly and comparative genomics of long-lived mammals reveal the common substitutions for cancer resistance.Aging cell · 2023Article
- RBM4 dictates ESCC cell fate switch from cellular senescence to glutamine-addiction survival through inhibiting LKB1-AMPK-axis.Signal transduction and targeted therapy · 2023Article
- LIM Kinases, LIMK1 and LIMK2, Are Crucial Node Actors of the Cell Fate: Molecular to Pathological Features.Cells · 2023Review
- SPHINX-Based Combination Therapy as a Potential Novel Treatment Strategy for Acute Myeloid Leukaemia.British journal of biomedical science · 2023Article
- Short-term hypoxia triggers ROS and SAFB mediated nuclear matrix and mRNA splicing remodeling.Redox biology · 2022Article
- Integration of TE Induces Cancer Specific Alternative Splicing Events.International journal of molecular sciences · 2022Review
- MiR-659-3p inhibits osteosarcoma progression and metastasis by inhibiting cell proliferation and invasion via targeting SRPK1.BMC cancer · 2022Article
- Increased expression of SRPK1 (serine/arginine-rich protein-specific kinase 1) is associated with progression and unfavorable prognosis in cervical squamous cell carcinoma.Bioengineered · 2022Article
- The distinct roles of zinc finger CCHC-type (ZCCHC) superfamily proteins in the regulation of RNA metabolism.RNA biology · 2021Review
- Oncogenic dysregulation of pre-mRNA processing by protein kinases: challenges and therapeutic opportunities.The FEBS journal · 2021Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Imbalanced splicing of premessenger RNA is typical of tumorous malignancies, and the regulatory mechanisms involved in several tumorigenesis-associated splicing events are identified. Elevated expression of serine-arginine protein kinase 1 (SRPK1) may participate in the pathway responsible for the dysregulation of splicing events in malignant tumor cells. In this study, we observed a correlation between the cytoplasmic accumulation of RNA-binding motif protein 4 (RBM4) and up-regulated SRPK1 in breast cancer cells. The production of the IR-B and MCL-1S transcripts was induced separately by the overexpression of RBM4 and SRPK1 gene silencing. Overexpressed RBM4 simultaneously bound to the CU-rich elements within the MCL-1 exon2 and the downstream intron, which subsequently facilitated the exclusion of the regulated exon. Breast cancer cells are deprived of apoptotic resistance through the RBM4-mediated up-regulation of the IR-B and MCL-1S transcripts. These findings suggest that the splicing events regulated by the SRPK1-RMB4 network may contribute to tumorigenesis through altered sensitivity to apoptotic signals in breast cancer cells.
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Registered trials
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.