Background Peroxisome proliferator‐activated receptor‐gamma (PPAR‐γ) activators have anti‐cancer effects. Our objective was to determine the effect of PPAR‐γ ligands 15‐deoxy‐D12,14‐Prostaglandin J2 (15‐PGJ2) and ciglitazone on proliferation, apoptosis, and NF‐κB in human oral squamous cell carcinoma cell lines. Methods NA and CA9‐22 cells were treated in vitro with 15‐PGJ2 and ciglitazone. Proliferation was measured by MTT colorimetric assay and cell cycle analysis performed via flow cytometry, apoptosis by caspase‐3 colorimetric assay and poly‐(ADP‐ribose) polymerase cleavage on Western blot, and NF‐κB activation by luciferase assays. Results MTT assays demonstrated dose‐dependent decreases after 15‐PGJ2 treatment in both cell lines, and S‐phase cell cycle arrest was also demonstrated. NF‐κB luciferase reporter gene activity decreased seven‐ and eightfold in NA and CA9‐22 cells, respectively. Caspase‐3 activity increased two‐ and eightfold in NA and CA9‐22 cells, respectively. Conclusions Our results suggest these agents, in addition to activating PPAR‐γ, can downregulate NF‐κB and potentiate apoptosis in oral cancer cells.

The coincubation of HNSCC with Cisplatin resulted in a decrease of about 50% at T24 and T48.Conclusion: DC pulsed with TL were able to present tumor antigens to lymphocytes resulting in the generation of tumor-specific CTL inducing tumor cell lysis. DC pulsed with TL may represent a method for inducing immune responses against squamous cell carcinomas of the upper aerodigestive tract.Significance: These results are encouraging for the possible application of pulsed DC in the therapy of HNSCC.