ArticleOncogene2017
Characterization of PTEN mutations in brain cancer reveals that pten mono-ubiquitination promotes protein stability and nuclear localization.
Article in Oncogene, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.
What it found
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Who cites it
63 citing papers in PubMed, 97 citations in OpenAlex.
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- Functionally deficient UBOX5 variants and primary angle-closure glaucoma.Nature communications · 2025Article
- Paired molecular profiling of malignant transformation of an epidermoid cyst for potential genetic drivers: illustrative case.Journal of neurosurgery. Case lessons · 2025Article
- SIRT7 facilitates endometrial cancer progression by regulating PTEN stability in an estrogen-dependent manner.Nature communications · 2025Article
- Deep learning prioritizes cancer mutations that alter protein nucleocytoplasmic shuttling to drive tumorigenesis.Nature communications · 2025Article
- Whole-genome sequencing analysis of Japanese autism spectrum disorder trios.Psychiatry and clinical neurosciences · 2025Article
- Genetically Engineered Brain Organoids Recapitulate Spatial and Developmental States of Glioblastoma Progression.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Network analyses of brain tumor multiomic data reveal pharmacological opportunities to alter cell state transitions.NPJ systems biology and applications · 2025Article
- Anticancer effect of the oncolytic Newcastle disease virus harboring the PTEN gene on glioblastoma.Oncology letters · 2025Article
- UBE2C-induced crosstalk between mono- and polyubiquitination of SNAT2 promotes lymphatic metastasis in bladder cancer.The Journal of clinical investigation · 2024Article
- Network Analyses of Brain Tumor Patients' Multiomic Data Reveals Pharmacological Opportunities to Alter Cell State Transitions.Research square · 2024Article
- Network Analyses of Brain Tumor Patients' Multiomic Data Reveals Pharmacological Opportunities to Alter Cell State Transitions.bioRxiv : the preprint server for biology · 2024Article
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- Mechanistic insights and the clinical prospects of targeted therapies for glioblastoma: a comprehensive review.Experimental hematology & oncology · 2024Review
- GRHL2-HER3 and E-cadherin mediate EGFR-bypass drug resistance in lung cancer cells.Frontiers in cell and developmental biology · 2024Article
- 'Slicing' glioblastoma drivers with the Swiss cheese model.Trends in cancer · 2024Review
- Liquid biopsy: creating opportunities in brain space.British journal of cancer · 2023Review
- Review
3 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
PTEN is a PIP3 phosphatase that antagonizes oncogenic PI3-kinase signalling. Due to its critical role in suppressing the potent signalling pathway, it is one of the most mutated tumour suppressors, especially in brain tumours. It is generally thought that PTEN deficiencies predominantly result from either loss of expression or enzymatic activity. By analysing PTEN in malignant glioblastoma primary cells derived from 16 of our patients, we report mutations that block localization of PTEN at the plasma membrane and nucleus without affecting lipid phosphatase activity. Cellular and biochemical analyses as well as structural modelling revealed that two mutations disrupt intramolecular interaction of PTEN and open its conformation, enhancing polyubiquitination of PTEN and decreasing protein stability. Moreover, promoting mono-ubiquitination increases protein stability and nuclear localization of mutant PTEN. Thus, our findings provide a molecular mechanism for cancer-associated PTEN defects and may lead to a brain cancer treatment that targets PTEN mono-ubiquitination.
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Registered trials
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