ArticleNeoplasia (New York, N.Y.)2005
SAK, a new polo-like kinase, is transcriptionally repressed by p53 and induces apoptosis upon RNAi silencing.
Article in Neoplasia (New York, N.Y.), 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 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
46 citing papers in PubMed, 81 citations in OpenAlex.
- Review
- Polo-like kinase 4 (PLK4) as a therapeutic target in breast cancer.Carcinogenesis · 2025Review
- Review
- Review
- Article
- The fate of extra centrosomes in newly formed tetraploid cells: should I stay, or should I go?Frontiers in cell and developmental biology · 2023Review
- Aberrant expression of polo-like kinase 4 in renal cell carcinoma: Association with clinicopathological characteristics and long-term survival.Oncology letters · 2022Article
- Hypoxia Drives Centrosome Amplification in Cancer Cells via HIF1α-dependent Induction of Polo-Like Kinase 4.Molecular cancer research : MCR · 2022Article
- Review
- Keep Calm and Carry on with Extra Centrosomes.Cancers · 2022Review
- PLK4 is a key molecule in the formation of PGCCs and promotes invasion and migration of progeny cells derived from PGCCs.Journal of Cancer · 2022Article
- Review
- Polo-Like Kinase 4's Critical Role in Cancer Development and Strategies for Plk4-Targeted Therapy.Frontiers in oncology · 2021Review
- Centrosome dysfunction: a link between senescence and tumor immunity.Signal transduction and targeted therapy · 2020Review
- PLK4: a promising target for cancer therapy.Journal of cancer research and clinical oncology · 2019Review
- Self-organization of Plk4 regulates symmetry breaking in centriole duplication.Nature communications · 2019Article
- Polo‑like kinase 4 promotes tumorigenesis and induces resistance to radiotherapy in glioblastoma.Oncology reports · 2019Article
- Once and only once: mechanisms of centriole duplication and their deregulation in disease.Nature reviews. Molecular cell biology · 2018Review
- Identification of Polo-like kinases as potential novel drug targets for influenza A virus.Scientific reports · 2017Article
- Plk1-mediated stabilization of 53BP1 through USP7 regulates centrosome positioning to maintain bipolarity.Oncogene · 2017Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chip profiling of a p53 temperature-sensitive tumor model identified SAK (Snk/Plk-akin kinase), encoding a new member of polo-like kinases (PLKs), as a gene strongly repressed by wild-type p53. Further characterization revealed that SAK expression was downregulated by wild-type p53 in several tumor cell models. Computer search of a 1.7-kb SAK promoter sequence revealed three putative p53 binding sites, but p53 failed to bind to any of these sites, indicating that SAK repression by p53 was not through a direct p53 binding to the promoter. Transcriptional analysis with luciferase reporters driven by SAK promoter deletion fragments identified SP-1 and CREB binding sites, which together conferred a two-fold SAK repression by p53. However, the repression was not reversed by cotransfection of SP-1 or CREB, suggesting a lack of interference between p53 and SP-1 or CREB. Significantly, p53-mediated SAK repression was largely reversed in a dose-dependent manner by Trichostatin A, a potent histone deacetylase (HDAC) inhibitor, suggesting an involvement of HDAC transcription repressors in SAK repression by p53. Biologically, SAK RNA interference (RNAi) silencing induced apoptosis, whereas SAK overexpression attenuated p53-induced apoptosis. Thus, SAK repression by p53 is likely mediated through the recruitment of HDAC repressors, and SAK repression contributes to p53-induced apoptosis.
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