ArticleScientific reports2025
The SREBF2-ACOT7 axis promotes tumor progression and predicts prognosis in diffuse large b-cell lymphoma.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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Who cites it
1 citing paper in PubMed.
- Acyl-CoA thioesterases and their derived lipid mediators: linking Acyl-CoA metabolic reprogramming to the tumor microenvironment.Frontiers in immunology · 2026Review
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Authors and funding
6 authors.
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Abstract
Diffuse large B-cell lymphoma (DLBCL) is the most common subtype of non-Hodgkin lymphoma, accounting for 30-40% of newly diagnosed cases globally. Although the R-CHOP regimen effectively cures 60-70% of patients, 30-40% of patients relapse or develop resistance, highlighting the need for new biomarkers to improve prognosis and therapeutic strategies. Members of the Acyl-CoA thioesterase (ACOT) family are known to regulate various cellular processes, including lipid metabolism, inflammation, and cancer progression. However, the role of ACOT7 in DLBCL remains unclear. In this study, we investigated the expression and function of ACOT7 in DLBCL. Using public database analysis and functional experiments, we found that ACOT7 is highly expressed in DLBCL tissues and is associated with poor patient prognosis. Silencing ACOT7 in DLBCL cell lines significantly inhibited cell proliferation, invasion, and regulated genes associated with epithelial mesenchymal transition (EMT), while promoting apoptosis and G0/G1 cell cycle arrest. Furthermore, we identified sterol regulatory element binding transcription factor 2 (SREBF2) as a transcriptional regulator of ACOT7, demonstrating that SREBF2 upregulates ACOT7 expression and promotes DLBCL progression. Our findings suggest that the SREBF2-ACOT7 axis plays a critical role in DLBCL by promoting tumor cell growth, invasion, and survival. ACOT7 could serve as a potential prognostic biomarker and therapeutic target for DLBCL, providing new insights into the molecular mechanisms of this aggressive lymphoma.
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