ArticleBMC cancer2024
TSA attenuates the progression of c-Myc-driven hepatocarcinogenesis by pAKT-ADH4 pathway.
Article in BMC cancer, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Why is the tumor microenvironment disordered by NADH/NADRedox biology · 2026Review
- Mitophagy-driven multidimensional regulation of tumor immune evasion and context-dependent therapeutic strategies.Journal of translational medicine · 2026Review
- Bioinformatics identification of key microRNA-correlated genes associated with hepatocellular carcinoma heterogeneity and prognosis.BMC gastroenterology · 2025Article
- From genes to therapy: a lipid Metabolism-Related genetic risk model predicts HCC outcomes and enhances immunotherapy.BMC cancer · 2025Article
- Alcohol-Metabolizing Enzymes, Liver Diseases and Cancer.Seminars in liver disease · 2025Review
- Exploration of the relationship between apoptosis related characteristic genes and the prognosis of HCC.Journal of Cancer · 2025Article
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Authors and funding
12 authors.
Funding
Abstract
Hepatocellular carcinoma (HCC) is the primary malignant tumor of the liver. c-Myc is one of the most common oncogenes in clinical settings, and amplified levels of c-Myc are frequently found in HCC. Histone deacetylase inhibitors (HDACi), such as Trichostatin A (TSA), hold enormous promise for the treatment of HCC. However, the potential and mechanism of TSA in the treatment of c-Myc-induced HCC are unclear. In this study, we investigated the effects of TSA treatment on a c-Myc-induced HCC model in mice. TSA treatment delayed the development of HCC, and liver function indicators such as ALT, AST, liver weight ratio, and spleen weight ratio demonstrated the effectiveness of TSA treatment. Oil red staining further demonstrated that TSA attenuated lipid accumulation in the HCC tissues of mice. Through mRNA sequencing, we identified that TSA mainly affected cell cycle and fatty acid degradation genes, with alcohol dehydrogenase 4 (ADH4) potentially being the core molecular downstream target. QPCR, immunohistochemistry, and western blot analysis revealed that ADH4 expression was repressed by c-Myc and restored after TSA treatment both in vitro and in vivo. Furthermore, we observed that the levels of total NAD
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