Trial reportInternational journal of molecular medicine2015
Activating transcription factor 3 is overexpressed in human glioma and its knockdown in glioblastoma cells causes growth inhibition both in vitro and in vivo.
Trial report in International journal of molecular medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 34 citations in OpenAlex.
- CBX6 and CA9 as predictive indicators and therapeutic targets in GBM.Molecular therapy. Oncology · 2026Article
- A comprehensive analysis of transcription factors identified TCF3 as a prognostic target for glioma.Scientific reports · 2025Article
- Activating transcription factor 3 induces oxidative stress and genotoxicity, transcriptionally modulating metastasis-related gene expression in human papillomavirus-infected cervical cancer.Virology journal · 2025Article
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- Changing paradigms in oncology: Toward noncytotoxic treatments for advanced gliomas.International journal of cancer · 2022Review
- UPF1/circRPPH1/ATF3 feedback loop promotes the malignant phenotype and stemness of GSCs.Cell death & disease · 2022Article
- Expression, Regulation, and Functions of the Galectin-16 Gene in Human Cells and Tissues.Biomolecules · 2021Article
- ATF3 contributes to brucine-triggered glioma cell ferroptosis via promotion of hydrogen peroxide and iron.Acta pharmacologica Sinica · 2021Article
- Scouting for common genes in the heterogenous hypoxic tumor microenvironment and their validation in glioblastoma.3 Biotech · 2021Article
- Time-Resolved Profiling Reveals ATF3 as a Novel Mediator of Endocrine Resistance in Breast Cancer.Cancers · 2020Article
- Expression, association with clinicopathological features and prognostic potential of CEP55, p-Akt, FoxM1 and MMP-2 in astrocytoma.Oncology letters · 2020Article
- Overexpression of activating transcription factor 3 exerts suppressive effects in HepG2 cells.Molecular medicine reports · 2019Article
- Activating transcription factor 3 promotes malignance of lung cancer cells in vitro.Thoracic cancer · 2017Article
- Cigarette smoke extract profoundly suppresses TNFα-mediated proinflammatory gene expression through upregulation of ATF3 in human coronary artery endothelial cells.Scientific reports · 2017Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glioblastomas are highly malignant gliomas that are extremely invasive with high rates of recurrence and mortality. It has been reported that activating transcription factor 3 (ATF3) is expressed in elevated levels in multiple malignant tumors. The purpose of this study was to investigate the function of ATF3 in the development of glioma and its clinical significance. Immunohistochemical staining, western blot analysis and RT-qPCR revealed that the mRNA and protein levels of ATF3 and matrix metalloproteinase 2 (MMP2) were higher in the glioma than in the normal human brain tissues, and that their levels were proportional to the pathological grades. By contrast, the mRNA and protein levels of mammary serine protease inhibitor (maspin; SERPINB5) were significantly lower in the glioma than in the normal brain tissue, and maspin expression was inversely proportional to the glioma pathological grade. The transfection of U373MG glioblastoma cells with ATF3-siRNA induced a number of changes in cell behavior; the cell proliferative activity was decreased and flow cytometry revealed an increased proportion of cells arrested in the G0/G1 phase of the cell cycle. In addition, TUNEL staining indicated an increased proportion of cells undergoing apoptosis and Transwell assays revealed impaired cell mobility. The sizes of the tumors grown as xenografts in nude mice were also significantly reduced by treatment of host mice with ATF3-siRNA. Taken together, these results suggest that ATF3 promotes the progression of human gliomas.
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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.