ArticleMolecular oncology2012
Genotoxic stress modulates CDC25C phosphatase alternative splicing in human breast cancer cell lines.
Article in Molecular oncology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
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Who cites it
12 citing papers in PubMed, 21 citations in OpenAlex.
- PUF60 promotes cell cycle and lung cancer progression by regulating alternative splicing of CDC25C.Cell reports · 2023Article
- Genome-wide screening identifies cell-cycle control as a synthetic lethal pathway with SRSF2P95H mutation.Blood advances · 2022Article
- Review
- Targeting Phosphatases and Kinases: How to Checkmate Cancer.Frontiers in cell and developmental biology · 2021Review
- Article
- Widespread alternative exon usage in clinically distinct subtypes of Invasive Ductal Carcinoma.Scientific reports · 2017Article
- Personalized characterization of diseases using sample-specific networks.Nucleic acids research · 2016Article
- The Expression and Clinical Outcome of pCHK2-Thr68 and pCDC25C-Ser216 in Breast Cancer.International journal of molecular sciences · 2016Article
- Myelodysplasia-associated mutations in serine/arginine-rich splicing factor SRSF2 lead to alternative splicing of CDC25C.BMC molecular biology · 2016Article
- Molecular mechanisms of etoposide.EXCLI journal · 2015Review
- The regulatory roles of phosphatases in cancer.Oncogene · 2014Review
- Genotoxic stress modulates CDC25C phosphatase alternative splicing in human breast cancer cell lines.Molecular oncology · 2012Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
CDC25 (cell division cycle 25) phosphatases are essential for cell cycle control under normal conditions and in response to DNA damage. They are represented by three isoforms, CDC25A, B and C, each of them being submitted to an alternative splicing mechanism. Alternative splicing of many genes is affected in response to genotoxic stress, but the impact of such a stress on CDC25 splicing has never been investigated. In this study, we demonstrate that genotoxic agents (doxorubicin, camptothecin, etoposide and cisplatin), alter the balance between CDC25C splice variants in human breast cancer cell lines both at the mRNA and protein levels. This modulation occurs during the response to moderate, sub-lethal DNA damage. Our results also suggest that the CDC25C splice variants expression shift induced by a genotoxic stress is dependent on the ATM/ATR signaling but not on p53. This study highlights the modulation of CDC25C alternative splicing as an additional regulatory event involved in cellular response to DNA damage 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.