ArticleNPJ precision oncology2024
Methionine deprivation inhibits glioma proliferation and EMT via the TP53TG1/miR-96-5p/STK17B ceRNA pathway.
Article in NPJ precision oncology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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The trial behind it
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Who cites it
7 citing papers in PubMed.
- LINC01446/miR-338-3p/APEX1 Axis Promotes Ferroptosis Defense and Progression in Esophageal Squamous Cell Carcinoma.Cancers · 2026Article
- Traditional Chinese Medicine-Derived Active Ingredient and Formulation Therapy for Glioma: Multi-Target Mechanisms, Drug Delivery Systems, and Advances in Clinical Translational Research.Pharmaceuticals (Basel, Switzerland) · 2026Review
- Emerging role of lncRNA TP53TG1 as a tumor regulator and biomarker in human malignancies.Discover oncology · 2026Review
- Tumor Electric Field Therapy Inhibits TGF-β/C1R Signaling Axis-Driven Epithelial-Mesenchymal Transition in Glioblastoma.CNS neuroscience & therapeutics · 2026Article
- Machine learning-integrated network toxicology uncovers glioma targets of DEHP.Frontiers in toxicology · 2026Article
- Role of autophagy‑modulating long non‑coding RNAs in tumor radioresistance (Review).Oncology reports · 2025Review
- Targeting TP53TG1: a promising prognostic biomarker and therapeutic target for personalized cancer therapy.Discover oncology · 2025Review
Corrections and comments
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Authors and funding
12 authors.
Funding
Abstract
Recent research highlights the significant impact of methionine metabolism on glioma progression. An increasing amount of compelling evidence bridges long non-coding RNAs to abnormal metabolism in gliomas. However, the specific role of long non-coding RNAs in methionine metabolism regulating glioma progression remains unclear. This study reveals that methionine deprivation inhibits the proliferation, migration, and invasion capabilities of gliomas. Interestingly, the expression of TP53TG1, a long non-coding RNA, is also suppressed. TP53TG1 is highly expressed in gliomas and associated with poor patient outcomes. Subsequently, our data proves that inhibition of TP53TG1 suppresses glioma cell proliferation and the epithelial-mesenchymal transition process both in vitro and in vivo. Ultimately, we found that the underlying mechanism involves a competing endogenous RNA regulating network, in which TP53TG1 modulates the target protein STK17B by competitively binding to miR-96-5p, thus regulating glioma progression. These findings suggest that targeting methionine deprivation could be a promising approach for the clinical treatment of glioma.
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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.