Integrated analysis of single cell and spatial transcriptomics revealed a metastasis mechanism mediated by fatty acid metabolism in lymph nodes of head and neck cancer
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View abstract on PubMed
Summary
This summary is machine-generated.Fatty acid metabolism, particularly involving LGALS1, drives head and neck squamous cell carcinoma (HNSCC) metastasis. Inhibiting LGALS1 reduces HNSCC cell proliferation and metastasis, offering potential therapeutic targets.
Area Of Science
- Oncology
- Molecular Biology
- Metabolism
Background
- Head and neck squamous cell carcinoma (HNSCC) is a prevalent malignancy.
- Tumor recurrence and metastasis significantly impact patient prognosis in HNSCC.
Purpose Of The Study
- To investigate the evolutionary mechanisms underlying HNSCC metastasis.
- To explore the role of fatty acid metabolism in HNSCC dissemination.
Main Methods
- Utilized single-cell RNA sequencing (scRNA-seq) and spatial transcriptome (ST) data.
- Performed pseudo-chronological, differentiation, cell interaction, and pathway analyses.
- Conducted in vivo and in vitro experiments to assess LGALS1 function.
Main Results
- Identified three subclusters: primary, transitional, and metastatic tumors.
- Observed upregulated fatty acid metabolism during tumor evolution, linked to LGALS1.
- Demonstrated that LGALS1 knockdown inhibits HNSCC proliferation, migration, and lymph node metastasis.
Conclusions
- Metabolic alterations, specifically in fatty acid metabolism, are crucial during HNSCC dissemination.
- Metastatic tumors play a key role in HNSCC metastasis mechanisms via fatty acid metabolism regulation.
- LGALS1 is a critical regulator of HNSCC metastasis, representing a potential therapeutic target.
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