Meta-Analysis Results on the Association Between TP53 Codon 72 Polymorphism With the Susceptibility to Oral Cancer.

Objectives: TP53 is an important tumor suppressor gene to maintain genomic integrity, and its mutations increase the susceptibility to oral carcinoma. Previous published studies have reported the relation of TP53 codon 72 polymorphism with the risk of oral carcinoma, but the results remain controversial and inconclusive. Methods: We therefore utilized meta-analysis based on a comprehensive search in PubMed, EMBASE, and Google of Scholar databases up to August 19, 2017. Results: Total 3,525 cases and 3,712 controls from 21 case-control studies were selected. We found no significant association between TP53 codon 72 polymorphism and oral carcinoma susceptibility in all genetic contrast models, including subgroup analysis based on control source and ethnicity. Furthermore, TP53 codon 72 polymorphism was not significant associated with oral carcinoma susceptibility in tobacco or alcohol use, and HPV infection status. Our results were confirmed by sensitivity analysis and no publication bias was found. Conclusions: Taken together, our data indicate that TP53 codon 72 polymorphism is not associated with the susceptibility to oral carcinoma.

Epigallocatechin­3­gallate inhibits the invasion of salivary adenoid cystic carcinoma cells by reversing the hypermethylation status of the RECK gene.

Epigallocatechin­3­gallate (EGCG) is an active and major constituent of green tea. As a non­nucleoside inhibitor of DNA methylation, EGCG is able to inhibit the hypermethylation of newly synthesised DNA, resulting in the reversal of hypermethylation and recovery in expression of the silenced genes. Reversion­inducing cysteine­rich protein with Kazal motifs (RECK) is a novel tumour suppressor gene, which negatively regulates matrix metalloproteinases, and inhibits tumour invasion, angiogenesis and metastasis. The present study aimed to examine the effects of EGCG on the methylation status of the RECK gene and tumour invasion in a salivary adenoid cystic carcinoma (SACC) cell line in vitro. Marked levels of methylated and weak levels of unmethylated RECK promoter were detected in the SACC83 cells, which was determined using methylation­specific polymerase chain reaction (PCR). In addition, the treatment of SACC83 cells with EGCG partially reversed the hypermethylation status of the RECK gene. Western blot analysis and reverse transcription­PCR demonstrated that EGCG significantly enhanced the protein and mRNA expression levels of RECK, and significantly reduced the invasive ability of the SACC83 cells, as determined using a Transwell assay. These results suggested that EGCG possesses novel anti­metastatic therapeutic potential for the treatment of SACC.

[The curative effects of bone mesenchymal stem cells transplanted into rats with Sjogren's syndrome].

PURPOSE: To study the curative effects, survival rate, migration and differentiation of bone mesenchymal stem cells (BMSCs) transplanted into rats with Sjogren's syndrome. METHODS: Model of Sjogren's syndrome was created in rats. BMSCs were isolated and cultured by using the preceding method. Then the pretreated BMSCs were identified and labeled by enhanced green fluorescent protein. BMSCs marked with enhanced green fluorescent protein (EGFP) or PBS were injected into the SMG of the Sjogren's syndrome rats via open surgery.Total static saliva flow rate was determined in rats. The daily amount of water in the normal group, the model group, the model treatment group and the model treatment control group was recorded. The survival rate, migration and differentiation of the BMSCs transplanted in the treatment group under fluorescence microscope was recorded. Student's t test was used for data analysis using SPSS 12.0 software package. RESULTS: Compared with the model treatment control group, the total static saliva flow rate of the model treatment group increased significantly, and the water they drank decreased significantly (P<0.05). In addition, BMSCs were distributed along the injection tract mostly in the first week,then BMSCs were mainly distributed in the stroma between the acinar in the second week and were distributed over other areas four weeks later. Immunohistochemical staining of amylzyme was not observed at the first week after transplantation. And at the 8th week the expression of amylzyme in the cytoplasm of the transplanted BMSCs was observed by immunohistochemical only in the model treatment group. CONCLUSION: Transplantation of BMSCs has certain treatment effect on Sjogren's syndrome.