ArticleCell death discovery2026
Lysophosphatidylcholine acyltransferase 1 promotes head and neck squamous cell carcinoma progression by enhancing COX17-dependent oxidative phosphorylation.
Article in Cell death discovery, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
1 citing paper in PubMed.
- Lysosomal lipid metabolism promotes tumor cell invasion through local energetics and membrane lipid remodeling.bioRxiv : the preprint server for biology · 2026Article
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Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Metabolic dysregulation is increasingly recognized as a driver of tumor progression, yet its specific role in head and neck squamous cell carcinoma (HNSCC) remains poorly characterized. This study integrated untargeted metabolomics of HNSCC patient tissues with multi-omics validation to identify key metabolic alterations. We discovered a significant accumulation of sn-2 saturated fatty acyl-phosphatidylcholines, implicating disrupted phospholipid remodeling in HNSCC pathogenesis. Analysis of The Cancer Genome Atlas and Human Protein Atlas databases revealed consistent upregulation of lysophosphatidylcholine acyltransferase 1 (LPCAT1) in HNSCC. This finding was further validated at mRNA, protein, and tissue levels by quantitative PCR, western blotting, and immunohistochemistry, respectively. Functional assays demonstrated that LPCAT1 knockdown suppressed tumor cell proliferation, migration, and invasion while increasing cell death in vitro, and inhibited tumor growth in nude mouse xenograft models. Mechanistically, LPCAT1 depletion impaired mitochondrial oxidative phosphorylation by reducing Cytochrome c oxidase activity, thereby decreasing ATP production. Our data further demonstrate that LPCAT1 regulates the expression of COX17, suggesting that the promotion of Cytochrome c oxidase activity and tumor bioenergetics by LPCAT1 is mediated through COX17. Thus, LPCAT1 drives HNSCC progression via a COX17-dependent metabolic reprogramming pathway. Targeting LPCAT1 represents a promising therapeutic strategy, while tissue-saturated fatty acyl-phosphatidylcholines may serve as early diagnostic biomarkers for HNSCC.
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Registered trials
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