ArticleScientific reports2017
Znf179 induces differentiation and growth arrest of human primary glioblastoma multiforme in a p53-dependent cell cycle pathway.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 6 papers, 1 of them a synthesis that pooled it.
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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, 16 citations in OpenAlex.
- Molecular Pathogenesis of Glioblastoma in Adults and Future Perspectives: A Systematic Review.International journal of molecular sciences · 2022Pooled it
- RNF112 Facilitates Ubiquitin-Mediated Degradation of c-Myc, Suppressing Proliferation, Migration and Lipid Synthesis in Bladder Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- RNF112, whose transcription is regulated by KLF4, inhibits colorectal cancer growth via promoting ubiquitin-dependent degradation of NAA40.Cell biology and toxicology · 2025Article
- Article
- Gene signatures and prognostic analyses of the Tob/BTG pituitary tumor-transforming gene (PTTG) family in clinical breast cancer patients.International journal of medical sciences · 2020Article
- Epigenetic Modification and Differentiation Induction of Malignant Glioma Cells by Oligo-Fucoidan.Marine drugs · 2019Article
Corrections and comments
- Erratum issued
Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Malignant glioblastoma multiforme (GBM) is an aggressive brain tumor with strong local invasive growth and a poor prognosis. One probable way to manipulate GBM cells toward a less invasive status is to reprogram the most malignant GBM cells to a more differentiated and less oncogenic phenotype. Herein, we identified a novel role of a RING finger protein Znf179 in gliomagenesis. Znf179 overexpression induced differentiation of primary GBM cells, which were accompanied with elevated glial fibrillary acidic protein (GFAP) expression through up-regulating several cell-cycle-related factors, p53, p21, and p27, and allowed the cell-cycle arrest in the G
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