鼻咽癌细胞中PPARγ、p-ERK、cyclin D1、Ki-67蛋白的表达及意义

Expression of PPARγ,p-ERK,cyclin D1 and Ki-67 proteins and their implication in nasopharyngeal carcinoma cells

目的探讨PPARγ、p-ERK、cyclin D1、Ki-67蛋白在鼻咽癌细胞中的表达关系及意义。方法应用免疫组织化学SP法检测36例鼻咽癌细胞和42例鼻咽黏膜慢性炎的鼻咽黏膜上皮细胞中PPARγ、p-ERK、cyclin D1、Ki-67蛋白的表达情况。结果36例鼻咽癌细胞中,PPARγ、p-ERK、cyclin D1、Ki-67阳性表达率分别为83.33%(30/36)、69.44%(25/36)、80.56%(29/36)、80.56%(29/36);42例鼻咽黏膜慢性炎的鼻咽黏膜上皮中阳性表达率分别为42.86%(18/42)、23.80%(10/42)、19.05%(8/42)、9.50%(4/42)。两组中PPARγ、p-ERK、cyclin D1、Ki-67蛋白的表达差异均有统计学意义(P<0.01)。36例鼻咽癌中,p-ERK与PPARγ、cyclin D1、Ki-67蛋白表达呈正相关(r=0.337,P<0.05;r=0.604,P<0.01;r=0.668,P<0.01);PPARγ与cyclin D1、Ki-67均无相关性(r=0.328,P>0.05;r=0.277,P>0.05)。结论鼻咽癌细胞中存在PPARγ、p-ERK、cyclin D1、Ki-67蛋白的高表达;鼻咽癌细胞中PPARγ可能参与p-ERK异常活化的正反馈调节;p-ERK可能通过上调cyclin D1和Ki-67的表达,促进鼻咽癌细胞增殖。

Purpose To investigate the relationship and significance of PPARγ,p-ERK,cyclin D1,and Ki-67 proteins expression in nasopharyngeal carcinoma cells（NPC）.Methods Immunohistochemical SP method was adopted to detect the expression of PPARγ,p-ERK,cyclin D1 and Ki-67 proteins in 36 cases of NPC and 42 chronic nasopharyngeal mucosal inflammation.Results Positive staining rates of PPARγ,p-ERK,cyclin D1,and Ki-67 proteins in 36 cases NPC were 83.33%（30/36）,69.44%（25/36）,80.56%（29/36）,and 80.56%（29/36）,respectively.Positive staining rates of the four proteins in 42 cases of nasopharyngeal mucosal inflammation were 42.86%（18/42）,23.80%（10/42）,19.05%（8/42）,and 9.50%（4/42）,respectively.The expression of PPARγ,p-ERK,cyclin D1,and Ki-67 proteins between the two groups had statistically significant differences（P0.01）.There were positive correlations between p-ERK and PPARγ,cyclin D1,and Ki-67 proteins expression in NPC（r=0.337,P0.05,r=0.604,P0.01,r=0.668,P0.01）.There were no correlations between PPARγ and cyclin D1,and Ki-67 proteins expression in NPC（r=0.328,P0.05;r=0.277,P0.05）.Conclusions Over expression of PPARγ,p-ERK,cyclin D1 and Ki-67 proteins exists in NPC.PPARγ may be regulated in a positive feedback manner with abnormally activated p-ERK in NPC cells.That p-ERK promots NPC cell proliferation may be through up-regulating cyclin D1 and Ki-67 proteins expression.