Knockdown of Cdc6 inhibits proliferation of tongue squamous cell carcinoma Tca8113 cells.

The present study aimed at evaluating the effects of Cdc6 downregulation on the proliferation of Tca8113 cells. Two lentiviral vectors (KD1 and KD2) expression cdc6 siRNA were constructed and then infected into Tca8113 cells. Real-time PCR and Western blot analysis were performed to detect the mRNA and protein expression of Cdc6. MTT assays were employed to delineate the growth curves, and flow cytometry was performed to assess cell-cycle progression and apoptosis in Tca8113 cells. Following infection with the lentiviral vectors, real-time PCR and Western blot analysis revealed that Cdc6 expression was markedly suppressed in Tca8113 cells. When compared with the negative control group, the mRNA expression of Cdc6 was reduced by 50% and 65% and the protein expression by 65.87% and 79.38% in cells harboring KD1 or KD2, respectively. Cell growth was slowed, and the growth inhibition rate was 25.84% and 30.34% in Tca8113 cells following infection with KD1 or KD2, respectively. In addition, cell-cycle progression was altered. In KD- infected Tca8113 cells, the proportion of cells in the S phase was markedly reduced, but the proportion in the G1 phase was significantly increased; this was accompanied by an increase in cell apoptosis. Downregulation of Cdc6 effectively inhibited the proliferation of Tca8113 cells.

Pulmonary metastases from an Ameloblastoma: case report and review of the literature.

Ameloblastomas have a high recurrence rate, and because of their biological tendency towards local invasion are considered borderline tumours. Despite this, reports of metastasis of these tumours are rare. This report presents a patient with mandibular ameloblastoma that recurred 29 years after surgery and metastasized to both lungs. Because of the large range of the area of metastasis, complete surgical resection of the tumours was impossible. After confirming the diagnosis by biopsy of the pulmonary lesions the pulmonary metastases were not treated actively. Observation over 4 years showed no obvious change in the lung metastasis. Recent cases are summarized and analyzed in this paper, with respect to its occurrence, pathological types, methods of treatment and other related aspects.

Spatio-temporal localization of HIF-1alpha and COX-2 during irradiation-induced oral mucositis in a rat model system.

PURPOSE: Oral mucositis is a common side effect of radiotherapy for head and neck cancer. The purpose of this study was to examine the significance of and the relationship between hypoxia inducible factor-1alpha (HIF-1alpha) and cyclooxygenase-2 (COX-2) gene expression and the corresponding protein levels in irradiated rat mucosa. MATERIAL AND METHODS: A Sprague-Dawley rat model of irradiation-induced oral mucositis was generated. Semi-quantitative reverse transcription-polymerase chain reaction (RT-PCR) was used to evaluate the HIF-1alpha and COX-2 mRNA level in rat buccal mucosa exposed to a fractionated irradiation regime. The Streptavidin-Biotin-Complex method was applied to delineate the in situ localization, intensity, and distribution of both proteins. The right buccal mucosa was not irradiated and used as control tissue. RESULTS: The RT-PCR analyses demonstrated that, upon irradiation, HIF-1alpha and COX-2 expression was significantly induced in the left buccal mucosa in contrast to control buccal mucosa. Based on immunohistochemical analyses, the HIF-1alpha and COX-2 level, in situ localization, and the type of cells exhibiting the highest HIF-1alpha and COX-2 amounts appear to correlate. CONCLUSIONS: The expression and protein levels of HIF-1alpha and COX-2 are substantially enhanced in irradiated rat mucosa and correlate with each other and with the severity of irradiation-induced oral mucositis.