ArticleNucleic acids research2012
Re-splicing of mature mRNA in cancer cells promotes activation of distant weak alternative splice sites.
Article in Nucleic acids research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 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.
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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
24 citing papers in PubMed, 31 citations in OpenAlex.
- Circular RNA Formation and Degradation Are Not Directed by Universal Pathways.International journal of molecular sciences · 2025Review
- Formation of Circular RNAs.Advances in experimental medicine and biology · 2025Review
- Advances in the understanding of circRNAs that influence viral replication in host cells.Medical microbiology and immunology · 2024Review
- CircAMOTL1 RNA and AMOTL1 Protein: Complex Functions ofInternational journal of molecular sciences · 2023Review
- Epstein-Barr Virus Enhances Cancer-Specific Aberrant Splicing of TSG101 Pre-mRNA.International journal of molecular sciences · 2022Article
- Review
- The Exon Junction Complex Core Represses Cancer-Specific Mature mRNA Re-splicing: A Potential Key Role in Terminating Splicing.International journal of molecular sciences · 2021Article
- Recent Advances in the Potential Use of Circular RNA for the Diagnosis and Treatment of Pancreatic Cancer.Cancer management and research · 2021Review
- Systematic Analyses of the Differentially Expressed Alternative Splicing Events in Gastric Cancer and Its Clinical Significance.Frontiers in genetics · 2020Article
- Cancer-Specifically Re-Spliced TSG101 mRNA Promotes Invasion and Metastasis of Nasopharyngeal Carcinoma.International journal of molecular sciences · 2019Article
- Research progress on circularRNAs in pancreatic cancer: emerging but promising.Cancer biology & therapy · 2019Review
- Research progress of circular RNAs in lung cancer.Cancer biology & therapy · 2019Review
- Normal and altered pre-mRNA processing in the DMD gene.Human genetics · 2017Review
- Circular RNAs: Biogenesis, Function, and a Role as Possible Cancer Biomarkers.International journal of genomics · 2017Review
- Circular RNAs-one of the enigmas of the brain.Neurogenetics · 2017Review
- Endogenous Multiple Exon Skipping and Back-Splicing at the DMD Mutation Hotspot.International journal of molecular sciences · 2016Article
- TSGΔ154-1054 splice variant increases TSG101 oncogenicity by inhibiting its E3-ligase-mediated proteasomal degradation.Oncotarget · 2016Article
- Non-sequential and multi-step splicing of the dystrophin transcript.RNA biology · 2016Article
- Novel transcription factor variants through RNA-sequencing: the importance of being "alternative".International journal of molecular sciences · 2015Article
- Allelic Imbalance of mRNA Associated with α2-HS Glycoprotein (Fetuin-A) Polymorphism.Disease markers · 2015Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Transcripts of the human tumor susceptibility gene 101 (TSG101) are aberrantly spliced in many cancers. A major aberrant splicing event on the TSG101 pre-mRNA involves joining of distant alternative 5' and 3' splice sites within exon 2 and exon 9, respectively, resulting in the extensive elimination of the mRNA. The estimated strengths of the alternative splice sites are much lower than those of authentic splice sites. We observed that the equivalent aberrant mRNA could be generated from an intron-less TSG101 gene expressed ectopically in breast cancer cells. Remarkably, we identified a pathway-specific endogenous lariat RNA consisting solely of exonic sequences, predicted to be generated by a re-splicing between exon 2 and exon 9 on the spliced mRNA. Our results provide evidence for a two-step splicing pathway in which the initial constitutive splicing removes all 14 authentic splice sites, thereby bringing the weak alternative splice sites into close proximity. We also demonstrate that aberrant multiple-exon skipping of the fragile histidine triad (FHIT) pre-mRNA in cancer cells occurs via re-splicing of spliced FHIT mRNA. The re-splicing of mature mRNA can potentially generate mutation-independent diversity in cancer transcriptomes. Conversely, a mechanism may exist in normal cells to prevent potentially deleterious mRNA re-splicing events.
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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.