ArticleCell death discovery2025
CRAT downregulation promotes ovarian cancer progression by facilitating mitochondrial metabolism through decreasing the acetylation of PGC-1α.
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 5 papers.
What it found
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The trial behind it
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Who cites it
5 citing papers in PubMed.
- Article
- Loss of CD90 alters EMT-associated features and drug sensitivity in U-CH1 chordoma cells.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Metabolomics Plasma Biomarkers Associated with the HRD Phenotype in Ovarian Cancer.Metabolites · 2025Article
- Androgen Receptors Promote Oxidative Phosphorylation and Resistance to Palmitate Lipotoxicity in ER-Mutant Breast Cancer.Endocrinology · 2025Article
- Cellular cAMP Content and Mitochondrial Profile Define Different Subtypes of Ovarian Cancer Cells.International journal of molecular sciences · 2025Article
Corrections and comments
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Authors and funding
11 authors.
Funding
Abstract
Mitochondrial dysfunctions are closely associated with different types of disease, including cancer. Carnitine acetyltransferase (CRAT) is a mitochondrial-localized enzyme catalyzing the reversible transfer of acyl groups from an acyl-CoA thioester to carnitine and regulates the ratio of acyl-CoA/CoA. Our bioinformatics analysis using public database revealed a significant decrease of CRAT expression in ovarian cancer (OC). However, the functions of CRAT have rarely been investigated in human cancers, especially in OC. Here, we found a frequent down-regulation of CRAT in OC, which is mainly caused by up-regulation of miR-132-5p. Downregulation of CRAT was significantly associated with shorter survival time for patients with OC. Forced expression of CRAT suppressed OC growth and metastasis by inducing cell cycle arrest and epithelial to mesenchymal transition (EMT). By contrast, CRAT knockdown promoted OC growth and metastasis. Mechanistically, we found that CRAT downregulation promoted OC growth and metastasis by increasing mitochondrial biogenesis to facilitate mitochondrial metabolism through reducing the acetylation of peroxisome proliferator-activated receptor-γ coactivator (PGC-1α). In summary, CRAT functions as a critical tumor suppressor in OC progression by enhancing PGC-1α-mediated mitochondrial biogenesis and metabolism, suggesting CRAT as a potential therapeutic target in treatment of OC.
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Registered trials
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