Expression of AEG-1 and microvessel density correlates with metastasis and prognosis of oral squamous cell carcinoma.

Astrocyte elevated gene 1 (AEG-1) expression is up-regulated in various human cancers and plays an important role in tumorigenesis and progression. The aim of this study was to explore AEG-1 expression in oral squamous cell carcinoma (OSCC) and to assess whether it is associated with microvessel density (MVD), metastasis, and survival. Specimens from 87 patients with OSCC were investigated by immunohistochemistry staining for AEG-1 and MVD. By statistical analysis, we studied the correlations between the expression of AEG-1 and MVD and various clinicopathological factors, including overall survival (OS). We found that AEG-1 was highly expressed in 51.72% of OSCC. Expression was closely correlated with differentiation, clinical stage, T classification, and lymph node metastasis. The MVD had similar results. Expression of AEG-1 correlated positively with MVD. The lymph node metastatic rate in patients with high AEG-1/high MVD was significantly higher than in patients with high AEG-1/low MVD, low AEG-1/high MVD, or low AEG-1/low MVD. Patients with high AEG-1 expression showed far lower OS rates than those with low expression. For MVD, there were similar results. Only AEG-1 and MVD expression were independent prognostic factors for OS by multivariate analysis. Expression of AEG-1 may be correlated with tumor angiogenesis and metastasis and is a valuable prognostic factor in patients with OSCC.

Vitapex can promote the expression of BMP-2 during the bone regeneration of periapical lesions in rats.

PURPOSE: To investigate the effect of Vitapex on the healing of periapical lesions and the expression of bone morphogenetic protein (BMP-2) during the periapical bone regeneration. MATERIALS AND METHODS: Periapical lesions were induced in Sprague-Dawley (S-D) rats by an occlusal pulp exposure in the mandibular first molars and were verified by X-ray. Total of 36 rats were randomly divided into three groups, and they were obturated with Zinc Oxide Eugenol (ZOE), or with Vitapex, or non-treated as negative control group. The rats of three groups were randomly killed at week 0, 2, 4, and 8 after root canal therapy, and then the mandibles were processed for histological examination and immunohistochemistry analysis. RESULTS: At week 0, only a few BMP-2 positive cells could be observed in all rats. While the expression of BMP-2 was dramatically increased in case of Vitapex group at week 2 and week 4, and then climaxed at week 8. However, no apparent changes were observed in ZOE group and negative group at week 2, 4, and 8. CONCLUSION: These observations suggested that Vitapex has a greater ability in inducing bone regeneration than ZOE by the expression of BMP-2 induction in the treatment of rats experimental periapical lesions.

The molecular mechanisms of the effect of Dexamethasone and Cyclosporin A on TLR4 /NF-κB signaling pathway activation in oral lichen planus.

Toll-like receptors (TLRs) and the nuclear factor-kappa B (NF-κB) signaling transduction pathway play important roles in the pathogenesis of several chronic inflammatory diseases, but its function in oral lichen planus (OLP) remains unclear. In this study, we examined the expression of TLR4 and NF-κB-p65 and inflammatory cytokines TNF-α and IL-1ß by immunohistochemistry in OLP tissues, and found that TLR4 and NF-κB-p65 were significantly upregulated in OLP compared to normal oral mucosa (P<0.05). We used keratinocytes HaCaT stimulated with lipopolysaccharide (LPS) to simulate the local OLP immune environment to some extent. RT-PCR and immunoblotting analyses showed significant activation of TLR4 and NF-κB-p65 in the circumstance of LPS-induced inflammatory response. The high expression of TLR4 and NF-κB-p65 are correlated with expression of cytokines TNF-α and IL-1ß (P<0.05). We further showed that NF-κB could act as an anti-apoptotic molecule in OLP. We conclude that TLR4 and the NF-κB signaling pathway may interact with the perpetuation of OLP. Steroids and cyclosporine are effective in the treatment of symptomatic OLP. However, there was some weak evidence for the mechanism over Dexamethasone (DeX) and Cyclosporine A (CsA) for the palliation of symptomatic OLP. In the present study, we found that Dexamethasone and Cyclosporine A negatively regulated NF-κB signaling pathway under LPS simulation in HaCaT cells by inhibiting TLR4 expression, on the other hand, Cyclosporine A could inhibit HaCaT cell proliferation by the induction of the apoptosis of HaCaT cells to protect OLP from the destruction of epidermal cells effectively.