ReviewOncotarget2019
Splicing regulatory factors in breast cancer hallmarks and disease progression.
Review in Oncotarget, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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
19 citing papers in PubMed.
- Tumoral switch in NUMB splicing changes essential transcription pathways and induces malignant properties in tumour cells.Genome biology · 2026Article
- Navigating luminal heterogeneity: etiology-based proteogenomic subtyping for targeted treatment strategies in breast cancer.Molecular cancer · 2026Article
- Assessment of SF3B1 Expression as a Prognostic Marker for Neoadjuvant Chemotherapy Response in Stage III Triple-Negative Breast Cancer.Reports of biochemistry & molecular biology · 2025Article
- A multi-tissue, splicing-based joint transcriptome-wide association study identifies susceptibility genes for breast cancer.American journal of human genetics · 2024Article
- Review
- PHF5A as a new OncoTarget and therapeutic prospects.Heliyon · 2023Review
- Learning from cancer to address COVID-19.Biologia futura · 2023Review
- SRSF5 Regulates the Expression of BQ323636.1 to Modulate Tamoxifen Resistance in ER-Positive Breast Cancer.Cancers · 2023Article
- Review
- Article
- Splicing alterations in healthy aging and disease.Wiley interdisciplinary reviews. RNA · 2021Review
- B7-H3 is spliced by SRSF3 in colorectal cancer.Cancer immunology, immunotherapy : CII · 2021Article
- Gene expression of adipokines and adipokine receptors in the tumor microenvironment: associations of lower expression with more aggressive breast tumor features.Breast cancer research and treatment · 2021Article
- Protein co-expression networks identified from HOT lesions of ER+HER2-Ki-67high luminal breast carcinomas.Scientific reports · 2021Article
- Alternative splicing modulates cancer aggressiveness: role in EMT/metastasis and chemoresistance.Molecular biology reports · 2021Review
- Prognostic Value and Potential Regulatory Mechanism of Alternative Splicing in Geriatric Breast Cancer.Genes · 2020Article
- Breast cancer in low-middle income countries: abnormality in splicing and lack of targeted treatment options.American journal of cancer research · 2020Review
- Alternative Splicing and CaV-Associated Channelopathies.Wiley interdisciplinary reviews. RNAReview
- PRKCSH Alternative Splicing Involves in Silica-Induced Expression of Epithelial-Mesenchymal Transition Markers and Cell Proliferation.Dose-response : a publication of International Hormesis SocietyArticle
Corrections and comments
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
By regulating transcript isoform expression levels, alternative splicing provides an additional layer of protein control. Recent studies show evidence that cancer cells use different splicing events to fulfill their requirements in order to develop, progress and metastasize. However, there has been less attention for the role of the complex catalyzing the complicated multistep splicing reaction: the spliceosome. The spliceosome consists of multiple sub-complexes in total comprising 244 proteins or splice factors and 5 associated RNA molecules. Here we discuss the role of splice factors in the oncogenic processes tumors cells need to fulfill their oncogenic properties (the so-called the hallmarks of cancer). Despite the fact that splice factors have been investigated only recently, they seem to play a prominent role in already five hallmarks of cancer: angiogenesis, resisting cell death, sustaining proliferation, deregulating cellular energetics and invasion and metastasis formation by affecting major signaling pathways such as epithelial-to-mesenchymal transition, the Warburg effect, DNA damage response and hormone receptor dependent proliferation. Moreover, we could relate expression of representative genes of four other hallmarks (enabling replicative mortality, genomic instability, avoiding immune destruction and evading growth suppression) to splice factor levels in human breast cancer tumors, suggesting that also these hallmarks could be regulated by splice factors. Since many splice factors are involved in multiple hallmarks of cancer, inhibiting splice factors might provide a new layer of oncogenic control and a powerful method to combat breast cancer progression.
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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.