ArticleOncology reports2016
Methylation-induced silencing of maspin contributes to the proliferation of human glioma cells.
Article in Oncology reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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.
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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
4 citing papers in PubMed, 8 citations in OpenAlex.
- Silencing Hmox1 Attenuates Cerebral Ischemia/reperfusion Injury and Inhibits Inflammation and Ferroptosis Via the PPAR-γ/FABP4 Signaling Pathway.Molecular neurobiology · 2025Article
- CDKN2A promoter methylation enhances self-renewal of glioblastoma stem cells and confers resistance to carmustine.Molecular biology reports · 2024Article
- A Novel Prognostic Signature Based on Glioma Essential Ferroptosis-Related Genes Predicts Clinical Outcomes and Indicates Treatment in Glioma.Frontiers in oncology · 2022Article
- Role of class I histone deacetylases in the regulation of maspin expression in prostate cancer.Molecular carcinogenesis · 2020Article
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Maspin, a member of the serpin superfamily of serine protease inhibitors, has been reported to be involved in cancer initiation and progression. However, the expression of maspin and its expression regulation in glioma remain unknown. In the present study, we aimed to investigate the function of maspin in glioma cells and its regulatory mechanism. We found that the expression of maspin was silenced in glioma cells and tissues. Although maspin had no effect on the migration and invasion of human glioma cells in vitro, overexpression of maspin inhibited cell growth in U87 cells. We showed that the methylase inhibitor 5-Aza-2'-deoxycytidine induced the expression of maspin in glioma cell lines. Furthermore, both U87 and U251 cells showed hypermethylation in the maspin promoter. In addition, bisulphite sequencing analysis indicated that 16 CpG sites in the promoter were completely methylated in glioma cells and cancerous tissues, while CpG dinucleotides in the maspin promoter were unmethylated in normal brain tissues. Our data suggest that methylation-induced silencing of maspin contributes to the proliferation of human glioma cells, and maspin may be a potential therapeutic target in glioma.
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Registered trials
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