ArticleJournal of cellular and molecular medicine2010
HDAC inhibitor, scriptaid, induces glioma cell apoptosis through JNK activation and inhibits telomerase activity.
Article in Journal of cellular and molecular medicine, 2010. 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
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Who cites it
28 citing papers in PubMed, 54 citations in OpenAlex.
- Acetylation modification in malignant progression and therapeutic resistance of gliomas.Frontiers in cell and developmental biology · 2026Review
- Epigenetic regulation of histone modifications in glioblastoma: recent advances and therapeutic insights.Biomarker research · 2025Review
- The histone deacetylase inhibitor Scriptaid targets G-quadruplexes.Open biology · 2025Article
- Article
- Electrochemical Synthesis of New Isoxazoles and Triazoles Tethered with Thiouracil Base as Inhibitors of Histone Deacetylases in Human Breast Cancer Cells.Molecules (Basel, Switzerland) · 2023Article
- Introducing HDAC-Targeting Radiopharmaceuticals for Glioblastoma Imaging and Therapy.Pharmaceuticals (Basel, Switzerland) · 2023Review
- TGIF1 overexpression promotes glioma progression and worsens patient prognosis.Cancer medicine · 2022Article
- Transcription Profile and Pathway Analysis of the Endocannabinoid Receptor Inverse Agonist AM630 in the Core and Infiltrative Boundary of Human Glioblastoma Cells.Molecules (Basel, Switzerland) · 2022Article
- The application of histone deacetylases inhibitors in glioblastoma.Journal of experimental & clinical cancer research : CR · 2020Review
- Review
- Anticancer effect of histone deacetylase inhibitor scriptaid as a single agent for hepatocellular carcinoma.Bioscience reports · 2018Article
- Potential Epigenetic-Based Therapeutic Targets for Glioma.Frontiers in molecular neuroscience · 2018Review
- MRGBP as a potential biomarker for the malignancy of pancreatic ductal adenocarcinoma.Oncotarget · 2017Article
- B1, a novel HDAC inhibitor, induces apoptosis through the regulation of STAT3 and NF-κB.International journal of molecular medicine · 2017Article
- Novel biomolecule lycopene-reduced graphene oxide-silver nanoparticle enhances apoptotic potential of trichostatin A in human ovarian cancer cells (SKOV3).International journal of nanomedicine · 2017Article
- Importance of rare gene copy number alterations for personalized tumor characterization and survival analysis.Genome biology · 2016Article
- Trichostatin A Enhances the Apoptotic Potential of Palladium Nanoparticles in Human Cervical Cancer Cells.International journal of molecular sciences · 2016Article
- Selective, potent blockade of the IRE1 and ATF6 pathways by 4-phenylbutyric acid analogues.British journal of pharmacology · 2013Article
- Is glioblastoma an epigenetic malignancy?Cancers · 2013Article
- Targeting of histone deacetylases in brain tumors.CNS oncology · 2013Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The present study identified a novel mechanism of induction of apoptosis in glioblastoma cells by scriptaid - a histone deacetylase (HDAC) inhibitor. Scriptaid reduced glioma cell viability by increasing Jun N-terminal kinase (JNK) activation. Although scriptaid induced activation of both p38MAPK and JNK, it was the inhibition of JNK that attenuated scriptaid-induced apoptosis significantly. Scriptaid also increased the expression of (i) p21 and p27 involved in cell-cycle regulation and (ii) γH2AX associated with DNA damage response in a JNK-dependent manner. Treatment with scriptaid increased Ras activity in glioma cells, and transfection of cells with constitutively active RasV12 further sensitized glioma cells to scriptaid-induced apoptosis. Scriptaid also inhibited telomerase activity independent of JNK. Taken together, our findings indicate that scriptaid (i) induces apoptosis and reduces glioma cell proliferation by elevating JNK activation and (ii) also decreases telomerase activity in a JNK-independent manner.
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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.