ArticleNucleic acids research2010
Genotoxic stress causes the accumulation of the splicing regulator Sam68 in nuclear foci of transcriptionally active chromatin.
Article in Nucleic acids research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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Who cites it
43 citing papers in PubMed, 77 citations in OpenAlex.
- Therapy-induced secretion of spliceosomal components mediates pro-survival crosstalk between ovarian cancer cells.Nature communications · 2024Article
- DNA Damage Regulates the Functions of the RNA Binding Protein Sam68 through ATM-Dependent Phosphorylation.Cancers · 2022Article
- Effective targeting of breast cancer stem cells by combined inhibition of Sam68 and Rad51.Oncogene · 2022Article
- Article
- Coordination of RNA Processing Regulation by Signal Transduction Pathways.Biomolecules · 2021Review
- Splicing alterations in healthy aging and disease.Wiley interdisciplinary reviews. RNA · 2021Review
- The splicing factor XAB2 interacts with ERCC1-XPF and XPG for R-loop processing.Nature communications · 2021Article
- Inhibition of HSF1 and SAFB Granule Formation Enhances Apoptosis Induced by Heat Stress.International journal of molecular sciences · 2021Article
- Stress Granules Involved in Formation, Progression and Metastasis of Cancer: A Scoping Review.Frontiers in cell and developmental biology · 2021Article
- Stress Granules in the Anti-Cancer Medications Mechanism of Action: A Systematic Scoping Review.Frontiers in oncology · 2021Article
- SAM68 promotes tumorigenesis in lung adenocarcinoma by regulating metabolic conversion via PKM alternative splicing.Theranostics · 2021Article
- RBM45 associates with nuclear stress bodies and forms nuclear inclusions during chronic cellular stress and in neurodegenerative diseases.Acta neuropathologica communications · 2020Article
- Alternative Splicing and DNA Damage Response in Plants.Frontiers in plant science · 2020Review
- Article
- TIAR marks nuclear G2/M transition granules and restricts CDK1 activity under replication stress.EMBO reports · 2019Article
- Alternative splicing in prostate cancer.Nature reviews. Clinical oncology · 2018Review
- Apoptotic Cell-Derived Extracellular Vesicles Promote Malignancy of Glioblastoma Via Intercellular Transfer of Splicing Factors.Cancer cell · 2018Article
- Clinical significance and effect of Sam68 expression in gastric cancer.Oncology letters · 2018Article
- Alternative polyadenylation of ZEB1 promotes its translation during genotoxic stress in pancreatic cancer cells.Cell death & disease · 2017Article
- miR‑30c suppresses prostate cancer survival by targeting the ASF/SF2 splicing factor oncoprotein.Molecular medicine reports · 2017Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
DNA-damaging agents cause a multifaceted cellular stress response. Cells set in motion either repair mechanisms or programmed cell death pathways, depending on the extent of the damage and on their ability to withstand it. The RNA-binding protein (RBP) Sam68, which is up-regulated in prostate carcinoma, promotes prostate cancer cell survival to genotoxic stress. Herein, we have investigated the function of Sam68 in this cellular response. Mitoxantrone (MTX), a topoisomerase II inhibitor, induced relocalization of Sam68 from the nucleoplasm to nuclear granules, together with several other RBPs involved in alternative splicing, such as TIA-1, hnRNP A1 and the SR proteins SC35 and ASF/SF2. Sam68 accumulation in nuclear stress granules was independent of signal transduction pathways activated by DNA damage. Using BrU labelling and immunofluorescence, we demonstrate that MTX-induced nuclear stress granules are transcriptionally active foci where Sam68 and the phosphorylated form of RNA polymerase II accumulate. Finally, we show that MTX-induced relocalization of Sam68 correlates with changes in alternative splicing of its mRNA target CD44, and that MTX-induced CD44 splicing depends on Sam68 expression. These results strongly suggest that Sam68 is part of a RNA-mediated stress response of the cell that modulates alternative splicing in response to DNA damage.
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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.