ArticleFEBS letters2022
The mitochondrial enzyme FAHD1 regulates complex II activity in breast cancer cells and is indispensable for basal BT-20 cells in vitro.
Article in FEBS letters, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 6 citations in OpenAlex.
- Catalytic activity of FAHD1 correlates with nuclear morphology and proteomic states in human osteosarcoma cells.Scientific reports · 2025Article
- FAHD1 and mitochondrial metabolism: a decade of pioneering discoveries.The FEBS journal · 2025Review
- Mitochondrial enzyme FAHD1 reduces ROS in osteosarcoma.Scientific reports · 2024Article
- A universal metabolite repair enzyme removes a strong inhibitor of the TCA cycle.Nature communications · 2024Article
- Roles of MT-ND1 in Cancer.Current medical science · 2023Review
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Authors and funding
11 authors at 4 institutions in 3 countries.
Funding
Abstract
The mitochondrial enzyme fumarylacetoacetate hydrolase domain-containing protein 1 (FAHD1) was identified to be upregulated in breast cancer tissues. Here, we show that FAHD1 is indispensable for the survival of BT-20 cells, representing the basal breast cancer cell type. A lentiviral knock-down of FAHD1 in the breast cancer cell lines MCF-7 and BT-20 results in lower succinate dehydrogenase (complex II) activity. In luminal MCF-7 cells, this leads to reduced proliferation when cultured in medium containing only glutamine as the carbon source. Of note, both cell lines show attenuated protein levels of the enzyme glutaminase (GLS) which activates programmed cell death in BT-20. These findings demonstrate that FAHD1 is crucial for the functionality of complex II in breast cancer cells and acts on glutaminolysis in the mitochondria.
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