ArticleMolecular biology reports2022
The novel histone deacetylase inhibitor pracinostat suppresses the malignant phenotype in human glioma.
Article in Molecular biology reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled it.
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.
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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
6 citing papers in PubMed, 1 synthesis or guideline pooled it, 10 citations in OpenAlex.
- Bibliometric and visualization analysis in the field of epigenetics and glioma (2009-2024).Frontiers in oncology · 2024Pooled it
- Benzimidazole motifs in drug discovery: sustainable synthetic strategies and emerging biological applications.RSC advances · 2026Review
- CuO nanoparticles for glioma treatment in vitro and in vivo.Scientific reports · 2024Article
- Biomarkers of Alzheimer's Disease Associated with Programmed Cell Death Reveal Four Repurposed Drugs.Journal of molecular neuroscience : MN · 2024Article
- Exploring the genetic causal association of TIMP3 on CKD and kidney function: a two-sample mendelian randomization.Frontiers in genetics · 2024Article
- Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
introductionGlioma is the most common malignant brain tumor in adults. The effects of conventional treatment regimens are still limited to prolonging the survival of patients. Histone deacetylases (HDACs) are potential targets for tumor treatment. Pracinostat is a new type of HDAC inhibitor (HDACi) that has a significant antitumor effect on a variety of tumors. Thus, we aim to investigate the role of pracinostat in human glioma and explored its underlying mechanism.
methodsCell viability, proliferation and apoptosis of human glioma cell lines were measured by Cell Counting kit 8 and flow cytometry. Pathway verification and protein interaction were determined by quantitative real-time polymerase chain reaction, Western blotting and immunofluorescence staining. Transwell technology was used to assess the migration and invasion of cells. Clinical significance of TIMP3, MMP9 and MMP2 in glioma was analyzed through The Cancer Genome Atlas (TCGA) database and the Genotype-Tissue Expression (GTEx) database.
resultsFunctionally, pracinostat not only inhibited proliferation and induced apoptosis but also inhibited migration and invasion in human glioma cell lines. Mechanistically, pracinostat increased the expression of TIMP3 and decreased the expression of MMP2, MMP9 and VEGF in human glioma cells in vitro and in vivo. In addition, pracinostat inhibited both the PI3K/Akt signaling pathway and the STAT3 pathway.
conclusionsOur results strongly support the potential clinical use of pracinostat as a novel therapy for human glioma in the near future.
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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.