ArticleCell journal2023
Down-Regulation of CEND1 Expression Contributes to The Progression and Temozolomide Resistance of Glioma.
Article in Cell journal, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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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Who cites it
3 citing papers in PubMed, 2 citations in OpenAlex.
- Neuronal differentiation regulator CEND1 coordinately suppresses tumor growth and energetics via AMPK signaling in brain glioma.Cell & bioscience · 2025Article
- Rapid and Effective Neuronal Conversion of Human Glioblastoma In Vitro and In Vivo Using Potent Small Molecules.Cell proliferation · 2025Article
- Pan-Cancer Analysis and Experimental Validation of CEND1 as a Prognostic and Immune Infiltration-Associated Biomarker for Gliomas.Molecular biotechnology · 2025Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveThis study was conducted to clarify the expression characteristics of cell cycle exit and neuronal differentiation 1 (CEND1) in glioma and its effects on the proliferation, migration, invasion, and resistance to temozolomide (TMZ) of glioma cells. MATERIALS AND
methodsIn this experimental study, CEND1 expression in glioma tissues and its relationship with patients' survival were analyzed through bioinformatics. Quantitative real-time polymerase chain reaction (qRT-PCR) and immunohistochemistry were performed to detect CEND1 expression in glioma tissues. The cell counting kit-8 (CCK-8) method was adopted to detect cell viability and the effects of different concentrations of TMZ on the inhibition rate of glioma cell proliferation, and the median inhibitory concentration of TMZ (IC
resultsCEND1 expression was reduced in glioma tissues and cells, and its low expression was significantly associated with the shorter survival of glioma patients. CEND1 knockdown promoted glioma cell growth, migration, and invasion, and increased the IC50 value of TMZ, whereas up-regulating CEND1 expression worked oppositely. Genes co-expressed with CEND1 were enriched in the NF-κB pathway, and knocking down CEND1 facilitated p-p65 expression, while CEND1 overexpression suppressed p-p65 expression.
conclusionCEND1 inhibits glioma cell proliferation, migration, invasion, and resistance to TMZ by inhibiting the NF- κB pathway.
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