Object: Hypoxia occurs when oxygen tension drops below normal limits, and malignant tumors often experience hy poxia, which activates the expression of genes through oxygen-sensitive transcription factors, including the hypoxia inducible factor (HIF) and the nuclear factor- κ B (NF- κ B). NF- κ B pathway represent s an attractive therapeutic target in both cancer cells and ischemic cells, which involv es immune response. To investigate the expression of NF- κ B target genes in oral squamous cancer carcinoma (OSCC) under hypoxia, we performed cDNA plate array analyses of 23 NF- κ B-regulated genes in different cell lines. Our aim was to clarify the functions of NF- κ B in OSCC under hypoxia. Results: We conducted an NF- κ B reporter assay to examine NF- κ B activation under hypoxia. This luciferase-based reporter assay showed that hypoxia induced NF- κ B activation after 24 h of hypoxia. We also found that vascular endo thelial growth factor-C (VEGF-C) of NF- κ B-regulated genes was upregulated in both cell lines under hypoxia. We then tested the influence of NF- κ B/p65 knockdown on these cells and NF- κ B/p65 knockdown inhibited the proliferation of OSCC cells by colony assay. Conclusion: Based on these findings, we postulate that one mechanism by which hypoxic OSCC cells may involve NF- κ B-mediated upregulation. Our results also indicate that the knockdown of NF- κ B/p65 subunit lead to growth inhibition during hypoxia in OSCC cells. These results suggest that knockdown of NF- κ B/p65 subunit could be a potential therapeutic option for patients with OSCC.
KeywordsOral Squamous Cell CarcinomaHypoxiaNF-κB
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