ArticleCell death & disease2024
DAP3 promotes mitochondrial activity and tumour progression in hepatocellular carcinoma by regulating MT-ND5 expression.
Article in Cell death & disease, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- MRPL3 enhances mitochondrial function via the TOMM40/PGC-1α/TFAM axis to drive early recurrence in hepatocellular carcinoma.Cell death & disease · 2026Article
- Article
- Targeting TM4SF1 promotes tumor senescence enhancing CD8+ T cell cytotoxic function in hepatocellular carcinoma.Clinical and molecular hepatology · 2025Article
- The construction and evaluation of a prognostic risk score model for HCC based on MPT-related lncRNAs.Frontiers in oncology · 2025Article
- Identification of DAP3 as candidate prognosis marker and potential therapeutic target for hepatocellular carcinoma.Frontiers in immunology · 2025Article
- Newly Established Anoikis-Associated Genes Predict the Prognosis of Hepatocellular Carcinoma.Journal of hepatocellular carcinoma · 2025Article
- Modulation of mProceedings of the National Academy of Sciences of the United States of America · 2024Article
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Authors and funding
11 authors.
Funding
Abstract
Cancer cells often exhibit fragmented mitochondria and dysregulated mitochondrial dynamics, but the underlying mechanism remains elusive. Here, we found that the mitochondrial protein death-associated protein 3 (DAP3) is localized to mitochondria and promotes the progression of hepatocellular carcinoma (HCC) by regulating mitochondrial function. DAP3 can promote the proliferation, migration, and invasion of HCC cells in vitro and in vivo by increasing mitochondrial respiration, inducing the epithelial-mesenchymal transition (EMT), and slowing cellular senescence. Mechanistically, DAP3 can increase mitochondrial complex I activity in HCC cells by regulating the translation and expression of MT-ND5. The phosphorylation of DAP3 at Ser185 mediated by AKT is the key event mediating the mitochondrial localization and function of DAP3 in HCC cells. In addition, the DAP3 expression in HCC samples is inversely correlated with patient survival. Our results revealed a mechanism by which DAP3 promotes mitochondrial function and HCC progression by regulating MT-ND5 translation and expression, indicating that DAP3 may be a therapeutic target for HCC.
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