ArticleOncogene2011
Phosphorylation by polo-like kinase 1 induces the tumor-suppressing activity of FADD.
Article in Oncogene, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
23 citing papers in PubMed, 38 citations in OpenAlex.
- CDK2-Mediated Phosphorylation ofResearch (Washington, D.C.) · 2026Article
- FADD Activation in Hepatocellular Carcinoma Potentiates CD8+ T-cell Responses and Sensitizes to Immune Checkpoint Inhibitors.Cancer research · 2025Article
- Fabrication and characterization of photosensitive non-isocyanate polyurethane acrylate resin for 3D printing of customized biocompatible orthopedic surgical guides.International journal of bioprinting · 2023Article
- A Dual Role for FADD in Human Precursor T-Cell Neoplasms.International journal of molecular sciences · 2022Article
- FADD as a key molecular player in cancer progression.Molecular medicine (Cambridge, Mass.) · 2022Review
- DED Interaction of FADD and Caspase-8 in the Induction of Apoptotic Cell Death.Journal of microbiology and biotechnology · 2022Article
- The Classical Apoptotic Adaptor FADD Regulates Glycolytic Capacity in Acute Lymphoblastic Leukemia.International journal of biological sciences · 2022Article
- Present and Future Perspective on PLK1 Inhibition in Cancer Treatment.Frontiers in oncology · 2022Review
- Identification of polo-like kinase 1 as a therapeutic target in murine lupus.Clinical & translational immunology · 2022Article
- RIPK1 and Caspase-8 Ensure Chromosome Stability Independently of Their Role in Cell Death and Inflammation.Molecular cell · 2019Article
- Article
- Structural insights of homotypic interaction domains in the ligand-receptor signal transduction of tumor necrosis factor (TNF).BMB reports · 2016Review
- Tumor suppressor genes and their underlying interactions in paclitaxel resistance in cancer therapy.Cancer cell international · 2016Review
- Determinants of eosinophil survival and apoptotic cell death.Apoptosis : an international journal on programmed cell death · 2015Review
- Sequential Cdk1 and Plk1 phosphorylation of caspase-8 triggers apoptotic cell death during mitosis.Molecular oncology · 2014Article
- Polo-like kinases (plks), a key regulator of cell cycle and new potential target for cancer therapy.Development & reproduction · 2014Article
- MicroRNA expressions associated with progression of prostate cancer cells to antiandrogen therapy resistance.Molecular cancer · 2014Article
- Increased Expression of Phosphorylated FADD in Anaplastic Large Cell and Other T-Cell Lymphomas.Biomarker insights · 2014Article
- The DUSP26 phosphatase activator adenylate kinase 2 regulates FADD phosphorylation and cell growth.Nature communications · 2014Article
- Pin1-FADD interactions regulate Fas-mediated apoptosis in activated eosinophils.Journal of immunology (Baltimore, Md. : 1950) · 2013Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Phosphorylation of the Fas-associated death domain (FADD) protein sensitizes cancer cells to various chemotherapeutics. However, the molecular mechanism underlying chemosensitization by phosphorylated FADD (P-FADD) is poorly understood. In this study, we describe the physical interactions and functional interplay between Polo-like kinase 1 (Plk1) and FADD. Plk1 phosphorylates FADD at Ser-194 in response to treatment with taxol. Overexpression of a phosphorylation-mimicking mutant, FADD S194D, caused degradation of Plk1 in an ubiquitin-independent manner, and delayed cytokinesis, consistent with the expected cellular phenotype of Plk1 deficiency. This demonstrates that Plk1 is regulated via a negative feedback loop by its substrate, FADD. Overexpression of FADD S194D sensitized HeLa cells to a low dose of taxol independently of caspase activation, whereas overexpression of FADD S194D resulted in caspase activation in response to a high dose of taxol. Therefore, we examined whether the death potential of P-FADD affected Plk1-mediated tumorigenesis. Transfection of FADD S194D inhibited colony formation by Plk1-overexpressing HeLa cells (HeLa-Plk1). Moreover, overexpression of FADD S194D suppressed tumorigenesis in nude mice xenografted with HeLa-Plk1. Therefore, this study reports the first in vivo validation of tumor-suppressing activity of P-FADD. Collectively, our data demonstrate that in response to taxol, Plk1 endows death-promoting and tumor-suppressor functions to its substrate, FADD.
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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.