ReviewOncology reviews2024
Post-Translational Modification of PTEN Protein: Quantity and Activity.
Review in Oncology reviews, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 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
12 citing papers in PubMed.
- The multifaceted significance of phosphoinositides in endocytic trafficking.FEBS letters · 2026Review
- PTEN restricts infectious bursal disease virus replication through modulating the AKT-TBK1-mediated type I IFN pathway.Poultry science · 2026Article
- RNF6 activates the AKT/mTOR signaling pathway by inhibiting PTEN via K27-linked polyubiquitination in myeloma.Acta pharmacologica Sinica · 2026Article
- Loss of PTEN as an Independent Poor Prognosis Indicator in Lung Adenocarcinoma, but Not in Squamous Cell Carcinoma, Is Associated with an Immunosuppressive Tumor Microenvironment and Distinct Co-Mutational Profiles.Medical sciences (Basel, Switzerland) · 2026Article
- UHRF2 related to sumoylation : assessment of its role in immune suppression and therapeutic potential in colorectal cancer.BMC cancer · 2026Article
- BiGKbhb: a bi-directional gated recurrent unit model for predicting lysine β-hydroxybutyrylation sites.BMC genomics · 2026Article
- Diabetic keratopathy and nuclear proteins (Review).Molecular medicine reports · 2026Review
- The cross-talk between GSK-3β, RKIP, and PTEN as potential targets for therapeutic implications in cancer: a comprehensive insight.Journal of pharmacy & pharmaceutical sciences : a publication of the Canadian Society for Pharmaceutical Sciences, Societe canadienne des sciences pharmaceutiques · 2026Review
- Ferroptotic resistance involved in PTEN-loss prostate cancer progression.Discover oncology · 2025Article
- Exploring Phosphatase and Tensin Homologue Deleted on Chromosome Ten (PTEN) as a Potential Therapeutic Target for Cardiac Hypertrophy.ACS pharmacology & translational science · 2025Review
- Review
- Sevoflurane Alleviates Cardiomyocyte Ferroptosis via Ubiquitin-Specific Protease 7/Phosphatase and Tensin Homolog Modulation.Drug design, development and therapy · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Post-translational modifications play crucial roles in regulating protein functions and stabilities. PTEN is a critical tumor suppressor involved in regulating cellular proliferation, survival, and migration processes. However, dysregulation of PTEN is common in various human cancers. PTEN stability and activation/suppression have been extensively studied in the context of tumorigenesis through inhibition of the PI3K/AKT signaling pathway. PTEN undergoes various post-translational modifications, primarily including phosphorylation, acetylation, ubiquitination, SUMOylation, neddylation, and oxidation, which finely tune its activity and stability. Generally, phosphorylation modulates PTEN activity through its lipid phosphatase function, leading to altered power of the signaling pathways. Acetylation influences PTEN protein stability and degradation rate. SUMOylation has been implicated in PTEN localization and interactions with other proteins, affecting its overall function. Neddylation, as a novel modification of PTEN, is a key regulatory mechanism in the loss of tumor suppressor function of PTEN. Although current therapeutic approaches focus primarily on inhibiting PI3 kinase, understanding the post-translational modifications of PTEN could help provide new therapeutic strategies that can restore PTEN's role in PIP3-dependent tumors. The present review summarizes the major recent developments in the regulation of PTEN protein level and activity. We expect that these insights will contribute to better understanding of this critical tumor suppressor and its potential implications for cancer therapy in the future.
Indexed as
Identifiers
What Socratic 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 Socratic graph.