Periodontal disease is a major oral disorder and comprises a group of infections that lead to inflammation of the gingiva and the destruction of periodontal tissues. PPARy plays an important role in the regulation of several metabolic pathways and has recently been implicated in inflammatory response pathways. However, its effects on periodontal inflammation have yet to be clarified. In our current study, we evaluated the anti-inflammatory effects of PPARy on periodontal disease. Human gingival fibroblasts (HGFs) treated with lipopolysaccharide (LPS) showed high levels of intracellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), matrix metalloproteinase-2 (MMP-2), and -9 (MMP-9). Moreover, these cells also showed upregulated activities for extracellular signal regulated kinase (ERK1/2), inducible nitric oxide synthase (iNOS) and cyclooxygnase-2. However, cells treated with Ad/PPARy and rosiglitazone in same culture system showed reduced ICAM-1, VCAM-1, MMP-2, -9 and COX-2. Finally, the anti-inflammatory effects of PPARy appear to be mediated via the suppression of the ERK1/2 pathway and consequent inhibition of NF-kB translocation. Our present findings thus suggest that PPARy indeed has a pivotal role in gingival inflammation and may be a putative molecular target for future therapeutic strategies to control chronic periodontal disease.

Inhibition of proteasome activity may reduce many types of cancer, so it's pathway is effective in cancer as well as in clinical fields. Here the author has carried out experiment targeting on the elevation of apoptosis in oral cancer cells by combination of proteasome inhibitor, lactacystin, and DNA replication inhibitor, etoposide. The growth of KB cells was measured by MTT methods and apoptosis was analyzed by DNA fragmentation and Hochest nucleus staining. The proteasome activity was analyzed by fluorescent tagged peptide and cellular protein expression was detected by Western hybridization. Though lactacystin and etoposide inhibited KB cell growth alone, but low combined doses inhibited cell growth more strongly and induced apoptosis. The proteasome activity was also seriously inhibited by the combination of both chemicals. Tumor suppressor proteins and apoptosis inducing proteins were highly increased under the combination of both chemicals. From above studies we can conclude that proteasome inhibitors may be used for the treatment of oral cancer and proteasome inhibitors with DNA replication inhibitors may be effective in clinical trials of oral cancer.

Oral squamous cell carcinoma (OSCC) is the most common malignancy and is a major cause of worldwide cancer mortality. The proto-oncogene c-myb plays an important role in regulation of cell growth and differentiation, and it is expressed at high levels in hematopoietic cells and many other types of cancers. However, the function of c-myb is not well known in OSCC. The present study aimed to reveal the function of c-myb and to test the alternation of cell growth and signaling by c-myb in OSCC. In this study, c-myb and dominant-negatibe myb(DNmyb) were expressed in an adenovirus-mediated gene delivery system to KB cells. The over-expressed c-myb brought increased cellular proliferation compared with control cells. However, DN-myb infected KB cells showed significant reduction of cell growth and enhanced induction of apoptosis to activate PARP and caspase 9. c-myb induced increase of IGF-I, -II and IGF-IR expressions while DN-myb down-regulated these expression. Activation of ERK and Akt/PKB pathway was shown only in c-myb transduced cells. These findings suggest that the role of c-myb in cell growth of oral cancer cells is partially mediated through the modulation of IGFs, ERK and Akt/PKB. From this results, DN-myb is strongly recommended as a curable gene for the treatment of c-myb dependent malignancies such as OSCC.