ReviewCell cycle (Georgetown, Tex.)2009
Hacking RNA: Hakai promotes tumorigenesis by enhancing the RNA-binding function of PSF.
Review in Cell cycle (Georgetown, Tex.), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
What it found
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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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
21 citing papers in PubMed, 35 citations in OpenAlex.
- Beyond destruction: emerging roles of the E3 ubiquitin ligase Hakai.Cellular & molecular biology letters · 2025Review
- Identifying human pre-mRNA cleavage and polyadenylation factors by genome-wide CRISPR screens using a dual fluorescence readthrough reporter.Nucleic acids research · 2024Article
- Established and Evolving Roles of the Multifunctional Non-POU Domain-Containing Octamer-Binding Protein (NonO) and Splicing Factor Proline- and Glutamine-Rich (SFPQ).Journal of developmental biology · 2024Review
- The Critical Role of RNA mCellular and molecular neurobiology · 2023Review
- Hakai is required for stabilization of core components of the mNature communications · 2021Article
- The role of RNAMolecular therapy. Nucleic acids · 2021Review
- PSF functions as a repressor of hypoxia-induced angiogenesis by promoting mitochondrial function.Cell communication and signaling : CCS · 2021Article
- Regulation of Epithelial-Mesenchymal Plasticity by the E3 Ubiquitin-Ligases in Cancer.Cancers · 2020Review
- Hakin-1, a New Specific Small-Molecule Inhibitor for the E3 Ubiquitin-Ligase Hakai, Inhibits Carcinoma Growth and Progression.Cancers · 2020Article
- CBLL1 is highly expressed in non-small cell lung cancer and promotes cell proliferation and invasion.Thoracic cancer · 2019Article
- Ajuba inhibits hepatocellular carcinoma cell growth via targeting of β-catenin and YAP signaling and is regulated by E3 ligase Hakai through neddylation.Journal of experimental & clinical cancer research : CR · 2018Article
- Hakai overexpression effectively induces tumour progression and metastasis in vivo.Scientific reports · 2018Article
- Non-nuclear Pool of Splicing Factor SFPQ Regulates Axonal Transcripts Required for Normal Motor Development.Neuron · 2017Article
- Human mesenchymal stem cell homing induced by SKOV3 cells.American journal of translational research · 2017Article
- Role of the microtubule-targeting drug vinflunine on cell-cell adhesions in bladder epithelial tumour cells.BMC cancer · 2014Article
- Posttranscriptional regulation by RNA-binding proteins during epithelial-to-mesenchymal transition.Cellular and molecular life sciences : CMLS · 2013Review
- Phosphotyrosine recognition domains: the typical, the atypical and the versatile.Cell communication and signaling : CCS · 2012Article
- Biological influence of Hakai in cancer: a 10-year review.Cancer metastasis reviews · 2012Review
- Article
- Reduced surface expression of epithelial E-cadherin evoked by interferon-gamma is Fyn kinase-dependent.PloS one · 2012Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Hakai, an E3 ubiquitin ligase for the E-cadherin complex, plays a crucial role in lowering cell-cell contacts in epithelial cells, a hallmark feature of tumor progression. Recently, Hakai was also found to interact with PSF (PTB-associated splicing factor). While PSF can function as a DNA-binding protein with a tumor suppressive function, its association with Hakai promotes PSF's RNA-binding ability and post-transcriptional influence on target mRNAs. Hakai overexpression enhanced the binding of PSF to mRNAs encoding cancer-related proteins, while knockdown of Hakai reduced the RNA-binding ability of PSF. Furthermore, the knockdown of PSF suppressed Hakai-induced cell proliferation. Thus, Hakai can affect the oncogenic phenotype both by altering E-cadherin-based intercellular adhesions and by increasing PSF's ability to bind RNAs that promote cancer-related gene expression.
Indexed as
Identifiers
What OpenQuestion holds
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.