Lactate dehydrogenase B as a metabolism-related marker for immunotherapy in head and neck squamous cell carcinoma
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View abstract on PubMed
Summary
This summary is machine-generated.Low lactate dehydrogenase B (LDHB) expression in head and neck squamous cell carcinoma (HNSCC) inhibits proliferation and improves immunotherapy response. This finding offers new insights into HNSCC tumor metabolism and immune interactions.
Area Of Science
- Oncology
- Cancer Metabolism
- Immunotherapy
Background
- Head and neck squamous cell carcinoma (HNSCC) is a prevalent malignancy.
- Lactate dehydrogenase family genes (LDHs) are crucial in tumor metabolism but underexplored in HNSCC.
Purpose Of The Study
- To comprehensively analyze the role and prognostic value of LDHs in HNSCC.
- To investigate the impact of LDHB on tumor cell proliferation, metabolism, and immune microenvironment.
Main Methods
- Utilized TCGA data for expression, mutation, methylation, and CNV analysis.
- Performed qPCR, immune infiltration analysis (ssGSEA, ESTIMATE, xCell, TIDE), and pathway enrichment (GO, GSEA, KEGG).
- Conducted in vitro assays (MTT, colony formation, ATP/lactate assays) and T cell differentiation studies.
Main Results
- LDHB was differentially expressed in HNSCC and associated with prognosis; low LDHB correlated with better clinicopathological features.
- Downregulated LDHB influenced tumor metabolism, enhanced immune cell infiltration, and predicted better response to immune checkpoint inhibitors (ICIs).
- LDHB knockdown inhibited proliferation, altered ATP/lactate levels, and promoted Th1 differentiation.
Conclusions
- Low LDHB expression inhibits HNSCC cell proliferation and ATP production via metabolic influence.
- Reduced LDHB is linked to improved immune cell infiltration and a more favorable response to immunotherapy in HNSCC.
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