ArticleOncogene2019
Inhibition of TAZ contributes radiation-induced senescence and growth arrest in glioma cells.
Article in Oncogene, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 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.
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Who cites it
26 citing papers in PubMed, 36 citations in OpenAlex.
- Article
- Exploring the potential anti-senescence effects of soybean-derived peptide Soymetide in mice hippocampal neurons via the Wnt/β-catenin pathway.Frontiers in pharmacology · 2025Article
- Overexpression of Growth Differentiation Factor 15 in Glioblastoma Stem Cells Promotes Their Radioresistance.Cancers · 2023Article
- An untapped window of opportunity for glioma: targeting therapy-induced senescence prior to recurrence.NPJ precision oncology · 2023Review
- Radiation-Induced Cellular Senescence Reduces Susceptibility of Glioblastoma Cells to Oncolytic Vaccinia Virus.Cancers · 2023Article
- Mechanical Properties of Glioblastoma: Perspectives for YAP/TAZ Signaling Pathway and Beyond.Diseases (Basel, Switzerland) · 2023Review
- The Molecular and Cellular Strategies of Glioblastoma and Non-Small-Cell Lung Cancer Cells Conferring Radioresistance.International journal of molecular sciences · 2022Review
- Effect of mechanical forces on cellular response to radiation.Radiotherapy and oncology : journal of the European Society for Therapeutic Radiology and Oncology · 2022Review
- Early Therapeutic Interventions for Newly Diagnosed Glioblastoma: Rationale and Review of the Literature.Current oncology reports · 2022Review
- Ferroptosis in Glioma Immune Microenvironment: Opportunity and Challenge.Frontiers in oncology · 2022Review
- The RNA binding protein QKI5 suppresses ovarian cancer via downregulating transcriptional coactivator TAZ.Molecular therapy. Nucleic acids · 2021Article
- Elimination of Radiation-Induced Senescence in the Brain Tumor Microenvironment Attenuates Glioblastoma Recurrence.Cancer research · 2021Article
- LncRNA MIR4435-2HG functions as a ceRNA against miR-125a-5p and promotes neuroglioma development by upregulating TAZ.Journal of clinical laboratory analysis · 2021Article
- Novel Strategies for Nanoparticle-Based Radiosensitization in Glioblastoma.International journal of molecular sciences · 2021Review
- Genome-wide CRISPR/Cas9 screening identifies CARHSP1 responsible for radiation resistance in glioblastoma.Cell death & disease · 2021Article
- B7-H3 suppresses doxorubicin-induced senescence-like growth arrest in colorectal cancer through the AKT/TM4SF1/SIRT1 pathway.Cell death & disease · 2021Article
- Hypoxia Transcriptomic Modifications Induced by Proton Irradiation in U87 Glioblastoma Multiforme Cell Line.Journal of personalized medicine · 2021Article
- Hippo Signaling Pathway in Gliomas.Cells · 2021Review
- The Paradoxical Role of Cellular Senescence in Cancer.Frontiers in cell and developmental biology · 2021Review
- A Small-Molecule Tankyrase Inhibitor Reduces Glioma Stem Cell Proliferation and Sphere Formation.Cancers · 2020Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
Glioblastoma (GBM) is the most aggressive brain tumor and resistant to current available therapeutics, such as radiation. To improve the clinical efficacy, it is important to understand the cellular mechanisms underlying tumor responses to radiation. Here, we investigated long-term cellular responses of human GBM cells to ionizing radiation. Comparing to the initial response within 12 hours, gene expression modulation at 7 days after radiation is markedly different. While genes related to cell cycle arrest and DNA damage responses are mostly modulated at the initial stage; immune-related genes are specifically affected as the long-term effect. This later response is associated with increased cellular senescence and inhibition of transcriptional coactivator with PDZ-binding motif (TAZ). Mechanistically, TAZ inhibition does not depend on the canonical Hippo pathway, but relies on enhanced degradation mediated by the β-catenin destruction complex in the Wnt pathway. We further showed that depletion of TAZ by RNAi promotes radiation-induced senescence and growth arrest. Pharmacological activation of the β-catenin destruction complex is able to promote radiation-induced TAZ inhibition and growth arrest in these tumor cells. The correlation between senescence and reduced expression of TAZ as well as β-catenin also occurs in human gliomas treated by radiation. Collectively, these findings suggested that inhibition of TAZ is involved in radiation-induced senescence and might benefit GBM radiotherapy.
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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.