ArticleCancer research2010
Genome-wide analysis of novel splice variants induced by topoisomerase I poisoning shows preferential occurrence in genes encoding splicing factors.
Article in Cancer research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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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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Who cites it
35 citing papers in PubMed, 57 citations in OpenAlex.
- The transcription factor c-Jun inhibits RBM39 to reprogram pre-mRNA splicing during genotoxic stress.Nucleic acids research · 2022Article
- Pancreatic cancer driver mutations are targetable through distant alternative RNA splicing dependencies.Oncotarget · 2021Article
- Alternative Splicing and DNA Damage Response in Plants.Frontiers in plant science · 2020Review
- Coupling of PARP1-mediated chromatin structural changes to transcriptional RNA polymerase II elongation and cotranscriptional splicing.Epigenetics & chromatin · 2019Article
- Article
- Environmental influences on RNA processing: Biochemical, molecular and genetic regulators of cellular response.Wiley interdisciplinary reviews. RNA · 2019Review
- Alternative-splicing defects in cancer: Splicing regulators and their downstream targets, guiding the way to novel cancer therapeutics.Wiley interdisciplinary reviews. RNA · 2018Review
- Article
- Therapy-induced stress response is associated with downregulation of pre-mRNA splicing in cancer cells.Genome medicine · 2018Article
- Environmental perturbations lead to extensive directional shifts in RNA processing.PLoS genetics · 2017Article
- Y14 governs p53 expression and modulates DNA damage sensitivity.Scientific reports · 2017Article
- Transcriptomic variation of pharmacogenes in multiple human tissues and lymphoblastoid cell lines.The pharmacogenomics journal · 2017Article
- Identification of several high-risk HPV inhibitors and drug targets with a novel high-throughput screening assay.PLoS pathogens · 2017Article
- Myelodysplasia-associated mutations in serine/arginine-rich splicing factor SRSF2 lead to alternative splicing of CDC25C.BMC molecular biology · 2016Article
- Article
- A genome landscape of SRSF3-regulated splicing events and gene expression in human osteosarcoma U2OS cells.Nucleic acids research · 2016Article
- A Novel Inhibitor of Topoisomerase I Is Selectively Toxic for a Subset of Non-Small Cell Lung Cancer Cell Lines.Molecular cancer therapeutics · 2016Article
- The RNA Splicing Response to DNA Damage.Biomolecules · 2015Review
- Genome-wide analysis of alternative transcripts in human breast cancer.Breast cancer research and treatment · 2015Article
- Role of the splicing factor SRSF4 in cisplatin-induced modifications of pre-mRNA splicing and apoptosis.BMC cancer · 2015Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
RNA splicing is required to remove introns from pre-mRNA, and alternative splicing generates protein diversity. Topoisomerase I (Top1) has been shown to be coupled with splicing by regulating serine/arginine-rich splicing proteins. Prior studies on isolated genes also showed that Top1 poisoning by camptothecin (CPT), which traps Top1 cleavage complexes (Top1cc), can alter RNA splicing. Here, we tested the effect of Top1 inhibition on splicing at the genome-wide level in human colon carcinoma HCT116 and breast carcinoma MCF7 cells. The RNA of HCT116 cells treated with CPT for various times was analyzed with ExonHit Human Splice Array. Unlike other exon array platforms, the ExonHit arrays include junction probes that allow the detection of splice variants with high sensitivity and specificity. We report that CPT treatment preferentially affects the splicing of splicing-related factors, such as RBM8A, and generates transcripts coding for inactive proteins lacking key functional domains. The splicing alterations induced by CPT are not observed with cisplatin or vinblastine and are not simply due to reduced Top1 activity, as Top1 downregulation by short interfering RNA did not alter splicing like CPT treatment. Inhibition of RNA polymerase II (Pol II) hyperphosphorylation by 5,6-dichloro-1-β-d-ribofuranosylbenzimidazole (DRB) blocked the splicing alteration induced by CPT, which suggests that the rapid Pol II hyperphosphorylation induced by CPT interferes with normal splicing. The preferential effect of CPT on genes encoding splicing factors may explain the abnormal splicing of a large number of genes in response to Top1cc.
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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.