ArticleInternational journal of oncology2025
Knockdown of ACC1 promotes migration and invasion of U251 glioma cells by epigenetically suppressing SDH.
Article in International journal of oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed.
- Gliomas with succinate dehydrogenase deficiency: A case series and brief review of the literature of oncometabolite-driven gliomagenesis.Journal of neuropathology and experimental neurology · 2026Review
- Metabolism of glioblastoma: a review of metabolic adaptations and metabolic therapeutic interventions.Frontiers in oncology · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glioma is a common and aggressive malignant brain tumor. Despite advances in research, the mechanisms driving glioma initiation and progression remain incompletely understood. The present study aimed to assess the role of acetyl‑CoA carboxylase 1 (ACC1) in glioma, focusing on its mechanistic function in U251 cells and its clinical significance. ACC1 expression was first assessed in four glioma cell lines and then the effects on cellular functions were evaluated. Based on the finding that ACC1 knockdown altered the phenotype of U251 cells, potentially through modulation of succinate dehydrogenase (SDH) activity, further mechanistic assessments were performed. Finally, the association between ACC1 expression and patient prognosis was analyzed. The results demonstrated that ACC1 overexpression inhibited proliferation, migration and invasion in U87 cells. Conversely, ACC1 knockdown promoted these processes in U251, T98G and LN229 cells. Mechanistically, in U251 cells, ACC1 knockdown increased acetyl‑CoA levels, enhancing substrate availability for P300. This led to upregulation of DNA methyltransferase 1 (DNMT1), hypermethylation of the SDH promoter and subsequent SDH downregulation. The resulting increase in reactive oxygen species (ROS) levels promoted U251 cell migration and invasion. Analysis of clinical data revealed a significant correlation between low ACC1 expression and poor survival outcomes in patients with glioma. These findings suggest that ACC1 functions as a tumor suppressor in glioma. Its downregulation promotes a pro‑tumorigenic phenotype via the acetyl‑CoA/P300/DNMT1/SDH/ROS pathway, highlighting its potential as a prognostic marker and therapeutic target. This underscores the importance of developing personalized treatment strategies targeting ACC1 in glioma.
Indexed as
Identifiers
What OpenQuestion holds
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.