ArticleCell death discovery2025
HADHA-mediated regulation of JAK/STAT3 signaling in glioblastoma: a metabolic-epigenetic axis.
Article in Cell death discovery, 2025. 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.
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.
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Who cites it
3 citing papers in PubMed.
- Intermediate accumulated upon interruption of fatty acid oxidation flux promotes tumoral ferroptosis and improves immunotherapy.Nature communications · 2026Article
- Reprogramming lipid metabolism in pediatric cancers.Oncogenesis · 2026Review
- Multi-omics profiling of sodium-overload (NECSO) programs identifies NEK8 as a central driver of colorectal cancer progression through single-cell and spatial transcriptomics.Frontiers in immunology · 2026Article
Corrections and comments
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Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
astractGlioblastoma multiforme (GBM) is one of the most aggressive forms of brain cancer, characterized by rapid growth and resistance to conventional therapies. This study investigates the role of HADHA, a key enzyme in fatty acid β-oxidation, in the progression of GBM. we show that the overexpression of HADHA in GBM correlates with a poor prognosis in patients and plays a role in promoting tumor growth and invasion. Mechanistically, HADHA regulates the JAK/STAT3 signaling pathway through modulation of H3K27ac histone acetylation. Knockdown of HADHA results in decreased acetyl-CoA levels, leading to reduced H3K27ac modification and subsequent inhibition of JAK/STAT3 activation. Furthermore, we show that the small molecule JIB-04, which targets HADHA, inhibits GBM cell proliferation and invasion both in vitro and in vivo. Our findings highlight the importance of targeting metabolic enzymes in cancer therapy and suggest that HADHA could represent a potential new therapeutic target for GBM. By targeting the metabolic-epigenetic pathway, this strategy presents a promising approach for treating this devastating disorder.
Identifiers
What Socratic 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 Socratic graph.