RESUMEN
Oral squamous cell carcinoma (OSCC) is a highly prevalent cancer worldwide, and OSCC often goes undiagnosed until advanced disease is present, which contributes to a low survival rate for OSCC patients. The identification of biomarkers for the early detection OSCC and novel therapeutic targets for OSCC treatment is an important research objective. We performed bioinformatics analyses of the gene expression profile of OSCC using microarray data to identify genes that contribute to the development of OSCC. We also predicted the transcription factors involved in the regulation of differential gene expression in OSCC. Our results showed that PI3K, EGFR, STAT1, and CPBP are important contributors to the changes in cellular physiology that occur during the development of OSCC. Therefore, these genes represent potential diagnostic biomarkers and therapeutic targets for OSCC.
RESUMEN
Inhibiting inflammation is helpful in relieving the absorption of alveolar bone and promoting periodontal bone regeneration. In a previous study, we showed that transforming growth factor-beta1 (TGF-ß1)-induced Treg cells inhibit the absorption of tissue-engineered cartilage caused by endogenous IFN-γ and TNF-α. In this study, we investigated the effect of inhibiting local inflammatory responses on Geistlich Bio-Oss® osteogenesis promotion in vivo. TGF-ß1+BMMSCs (bone marrow mesenchymal stem cells) were cultured in Geistlich Bio-Oss® medium, and biocompatibility was evaluated. Alveolar bone defects in New Zealand rabbits repaired by application of Geistlich Bio-Oss® were compared to the effects of added TGF-ß1+BMMSCs. There was no significant difference between the untreated Geistlich Bio-Oss® medium-control group and the group treated with the addition of TGF-ß1+BMMSCs. Pro-inflammatory cytokines IFN-γ and TNF-α delayed Geistlich Bio-Oss®-induced osteogenesis, but no significant difference in osteogenesis was seen with the addition of TGF-ß1+BMMSCs. Geistlich Bio-Oss® has good compatibility with TGF-ß1+BMMSCs. However, the dual role of in vivo TGF-ß1+BMMSCs in regenerating periodontal bone and limiting local inflammation is not clear.
RESUMEN
Aberrant histone deacetylase (HDAC) has a key role in the neoplastic process associated with the epigenetic patterns of tumor-related genes. The present study was performed to investigate the effects and determine the mechanism of action of the HDAC inhibitor, valproic acid (VPA), on the CAL27 cell line derived from oral squamous cell carcinoma (OSCC). The effects of VPA on the viability of CAL27 cells were investigated using MTT assays. Alterations in the cell cycle and apoptosis were also examined using propidium iodide (PI) and Annexin V-PI assays, and were subequently analyzed by flow cytometry. Small ubiquitin-related modifier (SUMO)-related genes were evaluated by reverse transcription-quantitative polymerase chain reaction analysis. In addition, the effects of VPA were assessed using a xenograft model in vivo. The present results demonstrated significant dose-dependent inhibition of cell viability following VPA treatment. Treatment with VPA increased the distribution of CAL27 cells in the G1 phase and reduced cells in the S phase, and significantly increased the expression levels of SUMO1 and SUMO2 (P<0.01). Using a xenograft model, the mean tumor volume in VPA-treated animals was demonstrated to be significantly reduced, and the rate of apoptosis was significantly increased, as compared with the control animals. These results suggested that VPA may regulate SUMOylation, producing an anticancer effect in vivo. Further investigation into the role of VPA in tumorigenesis may identify novel therapeutic targets for OSCC.