Loading
Life sciences · Journal article
Cell Death Discovery · September 14, 2026
No summary has been generated for this record yet. What follows is drawn from its source metadata only.
Journal article.
No findings were extractable from the material analysed.
Safety was not reported in the material analysed. Check the source before drawing any conclusion about harm.
The source did not state who this applies to in practice.
Graded across the dimensions that decide whether you should act, each from what the source actually supports. There is no single score, and where a dimension was not assessed it says so.
This record has not been graded across any dimension yet. Treat the label above as provisional and read the source.
What is missing. This record has no bottom line, key findings, reported figures, evidence dimensions. That is a gap in the analysis, not a judgement about the study.
Abstract Glioblastoma (GBM) is the most aggressive and lethal form of primary brain cancer in adults, characterized by rapid cell proliferation, resistance to therapy, and poor patient outcomes. While epigenetic dysregulation is increasingly recognized in glioma pathogenesis, the role of Histone Acetyltransferase 1 (HAT1) in GBM remains largely undefined. Here, we demonstrate that HAT1 expression is progressively reduced in high-grade gliomas of human tissue microarrays as well as in glioma cell lines with increased malignancy. We show that HAT1 depletion in glioma cells significantly enhances cell proliferation and membrane fluidity specifically in aggressive GBM subtypes (A172 and U87). Integrated transcriptomics and lipidomics analyses revealed upregulation of lipid metabolism pathways, including enhanced glycerophospholipid biosynthesis, alongside a marked induction of aldehyde dehydrogenase 2 (ALDH2) expression in HAT1-deficient cells. In contrast, HAT1 re-expression suppressed proliferation, restored membrane properties, and downregulated ALDH2. Subcutaneous xenograft models confirmed that HAT1 loss accelerates tumor growth, while HAT1 overexpression restrains it. Notably, knockdown of ALDH2 in HAT1-depleted GBM cells reversed the hyperproliferative and high-membrane-fluidity phenotype, identifying ALDH2 as a key downstream effector. Collectively, our data uncover a novel HAT1–ALDH2–lipid remodeling axis that regulates GBM cell proliferation and membrane plasticity, positioning HAT1 as a suppressor of GBM aggressiveness and highlighting this pathway as a potential axis for prognostic and therapeutic exploitation in GBM.