ReviewCancer metastasis reviews2012
Biological influence of Hakai in cancer: a 10-year review.
Review in Cancer metastasis reviews, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
28 citing papers in PubMed, 46 citations in OpenAlex.
- Exploring the Relationship Between Colitis-Associated Cancer and Lipid Metabolism Reprogramming from the Perspective of Inflammation-Cancer Transformation.Journal of inflammation research · 2026Review
- An mNature communications · 2025Article
- Bioinformatic Analysis of m6A Regulator-Mediated RNA Methylation Modification Patterns and Immune Microenvironment Characterization in Endometriosis.Biochemical genetics · 2025Article
- Beyond destruction: emerging roles of the E3 ubiquitin ligase Hakai.Cellular & molecular biology letters · 2025Review
- Role of the E3 ubiquitin-ligase Hakai in intestinal inflammation and cancer bowel disease.Scientific reports · 2022Article
- Celastrol inhibits the migration and invasion and enhances the anti-cancer effects of docetaxel in human triple-negative breast cancer cells.Medical oncology (Northwood, London, England) · 2022Article
- The roles of E3 ligases in Hepatocellular carcinoma.American journal of cancer research · 2022Review
- Cancer drug resistance induced by EMT: novel therapeutic strategies.Archives of toxicology · 2021Review
- Hakai is required for stabilization of core components of the mNature communications · 2021Article
- The emerging role of RNA N6-methyladenosine methylation in breast cancer.Biomarker research · 2021Review
- Role of Hakai in mNature communications · 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
- An oncopeptide regulates mNature communications · 2020Article
- Heat Shock Protein 90 Chaperone Regulates the E3 Ubiquitin-Ligase Hakai Protein Stability.Cancers · 2020Article
- E-cadherin might be a stage-dependent modulator in aggressiveness in pancreatic cancer cells.Turkish journal of biology = Turk biyoloji dergisi · 2020Article
- The role of ubiquitination and deubiquitination in the regulation of cell junctions.Protein & cell · 2018Review
- 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
- Basolateral CD147 induces hepatocyte polarity loss by E-cadherin ubiquitination and degradation in hepatocellular carcinoma progress.Hepatology (Baltimore, Md.) · 2018Article
- Hakai overexpression effectively induces tumour progression and metastasis in vivo.Scientific reports · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In order to metastasize, cancer cells must first detach from the primary tumor, migrate, invade through tissues, and attach to a second site. Hakai was discovered as an E3 ubiquitin-ligase that mediates the posttranslational downregulation of E-cadherin, a major component of adherens junctions in epithelial cells that is characterized as a potent tumor suppressor and is modulated during various processes including epithelial-mesenchymal transition. Recent data have provided evidences for novel biological functional role of Hakai during tumor progression and other diseases. Here, we will review the knowledge that has been accumulated since Hakai discovery 10 years ago and its implication in human cancer disease. We will highlight the different signaling pathways leading to the influence on Hakai and suggest its potential usefulness as therapeutic target for cancer.
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.