As a new group of important effector molecules involved in multiple cancer types, including breast cancer, lung cancer and oral squamous cell carcinoma, long noncoding RNAs (lncRNAs) have attracted considerable attention recently. However, the underlying cause that induces the dysregulated lncRNAs in cancer remains poorly understood. In the present study, the regulatory model of the lncRNA placenta-specific protein 2 (PLAC2) upregulation in oral squamous cell carcinoma (OSCC) was investigated and its biological functions in OSCC malignant progression was identified. A reverse transcription-quantitative polymerase chain reaction assay identified that PLAC2 is upregulated in OSCC cell lines and primary tissue samples. Furthermore, bioinformatic analysis followed by chromatin immunoprecipitation verified an enriched histone H3 on lysine 27 (H3K27) acetylation (H3K27ac) at the promoter region of the PLAC2 gene. Knockdown of cAMP-response element binding protein-binding protein (CBP) significantly reduced the enrichment level of H3K27ac, and thereby induced a decreased expression of PLAC2. Functionally, overexpression of PLAC2 promotes OSCC cell proliferation, migration and invasion, whereas knockdown of PLAC2 exerted an opposite effect. Furthermore, the Wnt/β-catenin signaling pathway was activated by PLAC2 and mediated the PLAC2-induced malignant progress of OSCC. In conclusion, the present results indicated that lncRNA PLAC2 is transcriptionally activated by H3K27ac modification at the promoter region in OSCC, and promotes cell growth and metastasis via activating Wnt/β-catenin signaling pathway. Therefore, PLAC2 may serve as a promising biomarker for OSCC prognosis and therapy.

The purpose of this study was to investigate how cyclic loading influenced the fracture toughness of hot-press lithium disilicate and zirconia core materials and whether there was an increase in the propensity for crown failure. Two types of all-ceramic crowns including the IPS e.max Press system (n=24) and the Lava zirconia system (n=24), were selected. Sectioned specimens were subjected to cyclic loading with the maximum magnitude of 200 N (R=0.1) until two million cycles. The material properties including Young's modulus (E) and hardness (H) and the fracture toughness (KIC) of the core materials were evaluated using indentation methods (n=12 each). The load-bearing capacities of the specimens were examined by means of monotonic load to fracture (n=12 each). It was found that the material properties, including E, H and KIC, of the two types of dental ceramics, were reduced. Statistical analysis indicated that there were no significant influences of fatigue loading on material properties E and H for both types of dental ceramics or KIC for zirconia, while for the IPS e.max Press core, KIC, which was parallel to the direction of the lithium disilicate crystals, was significantly reduced (P=0.001). A conclusion was drawn that zirconia possesses high mechanical reliability and sustainable capacity to resist fatigue loading, while fatigue loading remarkably degraded the anisotropic mechanical behaviour of hot-press lithium disilicate ceramics.

Hypodontia is caused by interactions among genetic, epigenetic, and environmental factors during tooth development, but the actual mechanism is unknown. DNA methylation now appears to play a significant role in abnormal developments, flawed phenotypes, and acquired diseases. Methylated DNA immunoprecipitation (MeDIP) has been developed as a new method of scanning large-scale DNA-methylation profiles within particular regions or in the entire genome. Here, we performed a genome-wide scan of paired DNA samples obtained from 4 patients lacking two mandibular incisors and 4 healthy controls with normal dentition. We scanned another female with non-syndromic anodontia and her younger brother with the same gene mutations of the PAX9,MSX1,AXIN2 and EDA, but without developmental abnormalities in the dentition. Results showed significant differences in the methylation level of the whole genome between the hypodontia and the normal groups. Nine genes were spotted, some of which have not been associated with dental development; these genes were related mainly to the development of cartilage, bone, teeth, and neural transduction, which implied a potential gene cascade network in hypodontia at the methylation level. This pilot study reveals the critical role of DNA methylation in hypodontia and might provide insights into developmental biology and the pathobiology of acquired diseases.