RANKL、OPG、NF-κBp65蛋白表达在牙龈癌中临床意义

Expression of RANKL,OPG,NF-κBp65 Protein in Gingival Carcinoma and Its Clinical Significance

目的观察牙龈癌中RANKL、OPG、NF-κBp65蛋白表达和RANKL/OPG比值变化,初步探讨骨质破坏相关蛋白所代表的生物学行为和临床意义。方法收集2018年7月~2019年12月笔者医院牙龈癌临床标本,采用免疫组织化学方法检测RANKL、OPG、NF-κBp65蛋白表达并分析RANKL/OPG比值变化。通过Western blot法比较体外培养的牙龈癌和牙龈上皮细胞中3种蛋白表达及RANKL/OPG比值差异。结果牙龈癌临床标本中,RANKL和OPG蛋白在细胞质中强阳性表达,NF-κBp65在细胞核中强阳性表达,对照组弱阳性表达,实验组与对照组比较,差异有统计学意义(P<0.05),RANKL/OPG比值较对照组升高,差异有统计学意义(P<0.05)。Western blot法结果显示,与牙龈上皮细胞比较,牙龈癌细胞中RANKL、OPG、NF-κBp65蛋白过表达,RANKL/OPG比值升高,差异有统计学意义(P<0.05)。结论 RANKL、OPG蛋白表达及RANKL/OPG比值升高后可能通过激活NF-κBp65引起牙龈上皮细胞异常分化为牙龈癌细胞,为牙龈癌发病机制探讨及临床治疗靶点选择提供新的实验依据。

Objective To detect the expression ofRANKL,OPG,NF-κBp65 protein in gingival carcinoma,and to observe the change of RANKL/OPG ratio,then to investigate the biological behavior and clinical significance of bone destruction associated protein.Methods The expression of RANKL,OPG and NF-κBp65 protein was detected by immunohistochemical method in the clinical specimens of gingival carcinoma from July 2018 to December 2019,and RANKL/OPG ratio was analyzed.Western blot was used to compare the expression of three proteins in human gingival cancer cells and gingival epithelial cells,and to analyze the RANKL/OPG ratio.Results In the clinical specimens of gingival carcinoma,RANKL and OPG were strongly positive in the cytoplasm,NF-κBp65 was strongly positive in the nuclei.The control group was weakly positive by immunohistochemical staining.Compared with the control group,the experimental group had statistical significance(P<0.05).The ratio of RANKL/OPG was significantly higher than that of control group(P<0.05).Western blot analysis showed that RANKL,OPG,NF-κBp65protein overexpression and RANKL/OPG ratio was significantly higher in gingival cancer cells than in gingival epithelial cells,the results were statistically significant(P<0.05).Conclusion The increased expression of RANKL,OPG and RANKL/OPG ratio may induce abnormal differentiation of gingival epithelial cells into gingival cancer cells by activating NF-κBp65,which provides a new experimental basis for the study of the pathogenesis of gingival cancer and the selection of clinical therapeutic targets.