ArticleCell death & disease2014
Depletion of pre-mRNA splicing factor Cdc5L inhibits mitotic progression and triggers mitotic catastrophe.
Article in Cell death & disease, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
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Who cites it
45 citing papers in PubMed, 83 citations in OpenAlex.
- RSRC2 is a novel RNA-binding protein that safeguards mitotic fidelity by interacting with the lncRNA C1QTNF1-AS1.Nucleic acids research · 2026Article
- Proteomic analysis of the zone of degeneration at the mitosis-meiosis transition stage in wild-caught male catshark (Scyliorhinus canicula), correlated with an unusually high-water temperature in the English Channel.Journal of fish biology · 2026Article
- Splicing as an integrative layer linking cell cycle regulation, epigenetic dynamics, and environmental responses in plants.Frontiers in plant science · 2026Review
- DNA repair pathway-related proteins are involved in the circularization step of microDNA eccDNACommunications biology · 2025Article
- Targeting HASPIN kinase disrupts SR protein-mediated RNA splicing and synergizes with BCL-2 inhibitor venetoclax in AML.Blood neoplasia · 2025Article
- Deletion of splicing factor Cdc5 in Toxoplasma disrupts transcriptome integrity, induces abortive bradyzoite formation, and prevents acute infection in mice.Nature communications · 2025Article
- Prp19/CDC5L promotes gastric cancer via activation of the MAPK pathway-mediated homologous recombination.International journal of biological sciences · 2025Article
- EIF4A3 Promotes Cell Proliferation via CDC5L Upregulation in Human Breast Cancer Cells.Journal of Cancer · 2025Article
- Nanomedicine-induced programmed cell death in cancer therapy: mechanisms and perspectives.Cell death discovery · 2024Review
- Deregulated circRNAs in Epithelial Ovarian Cancer With Activity in PreclinicalCancer genomics & proteomics · 2024Review
- Review
- DHX34 as a promising biomarker for prognosis, immunotherapy and chemotherapy in Pan-Cancer: A Comprehensive Analysis and Experimental Validation.Journal of Cancer · 2024Article
- mAmerican journal of cancer research · 2024Article
- FOXA1 prolongs S phase and promotes cancer progression in non-small cell lung cancer through upregulation of CDC5L and activation of the ERK1/2 and JAK2 pathways.The Kaohsiung journal of medical sciences · 2023Article
- Elevated level of PLRG1 is critical for the proliferation and maintenance of genome stability of tumor cells.BMB reports · 2023Article
- The emerging significance of splicing in vertebrate development.Development (Cambridge, England) · 2022Review
- The Interplay of Cohesin and RNA Processing Factors: The Impact of Their Alterations on Genome Stability.International journal of molecular sciences · 2022Review
- New insights into phenotypic heterogeneity for the distinct lipid accumulation of Schizochytrium sp. H016.Biotechnology for biofuels and bioproducts · 2022Article
- The PRP19 Ubiquitin Ligase, Standing at the Cross-Roads of mRNA Processing and Genome Stability.Cancers · 2022Review
- Pan-Cancer Transcriptome and Immune Infiltration Analyses Reveal the Oncogenic Role of Far Upstream Element-Binding Protein 1 (FUBP1).Frontiers in molecular biosciences · 2022Article
Corrections and comments
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Authors and funding
17 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Disturbing mitotic progression via targeted anti-mitotic therapy is an attractive strategy for cancer treatment. Therefore, the exploration and elucidation of molecular targets and pathways in mitosis are critical for the development of anti-mitotic drugs. Here, we show that cell division cycle 5-like (Cdc5L), a pre-mRNA splicing factor, is a regulator of mitotic progression. Depletion of Cdc5L causes dramatic mitotic arrest, chromosome misalignments and sustained activation of spindle assembly checkpoint, eventually leading to mitotic catastrophe. Moreover, these defects result from severe impairment of kinetochore-microtubule attachment and serious DNA damage. Genome-wide gene expression analysis reveals that Cdc5L modulates the expression of a set of genes involved in the mitosis and the DNA damage response. We further found that the pre-mRNA splicing efficiency of these genes were impaired when Cdc5L was knocked down. Interestingly, Cdc5L is highly expressed in cervical tumors and osteosarcoma. Finally, we demonstrate that downregulation of Cdc5L decreases the cell viability of related tumor cells. These results suggest that Cdc5L is a key regulator of mitotic progression and highlight the potential of Cdc5L as a target for cancer therapy.
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