磷酸化p38促分裂原活化的蛋白激酶、尿激酶型纤溶酶原激活物及Ki-67在牙源性上皮性肿瘤中的表达

目的 检测磷酸化p38促分裂原活化的蛋白激酶(phosphorylated-p38 mitogen-activated protein kinase,p-p38MAPK)、尿激酶型纤溶酶原激活物(urokinase plasminogen activator,uPA)及Ki-67在牙源性上皮性肿瘤中的表达,探讨p-p38MAPK对牙源性上皮性肿瘤细胞增殖活性及侵袭性的影响.方法 根据2005年WHO关于牙源性肿瘤的分类标准,应用免疫组化方法检测p-p38MAPK、uPA和Ki-67在成釉细胞瘤(ameloblastoma,AB)、牙源性角化囊性瘤(keratocystic odontogenic tumour,KCOT)、牙源性钙化上皮瘤(calcifying epithelial odontogenic tumor,CEOT)、牙源性腺样瘤(adenomatoid odontogenic tumour,AOT)及牙源性钙化囊性瘤(calcifying cystic odontogenic tumour,CCOT)(以上为肿瘤组)和5例牙胚(对照组)中的表达.结果 p-p38MAPK在肿瘤组的阳性表达率为26%(17/65),在肿瘤细胞胞质和胞核均可见着色;uPA在肿瘤组的阳性表达率为78%(51/65),主要表现为肿瘤细胞胞质着色;Ki-67在肿瘤组的阳性表达率为95%(62/65),为弥散的肿瘤细胞胞核着色.p-p38MAPK、uPA和Ki-67在牙源性上皮性肿瘤的阳性表达率显著高于对照组(P＜0.05),三者的阳性表达呈正相关(P＜0.05).结论 p-p38MAPK信号传导通路可能以正性调节的方式调控uPA从而促进牙源性上皮性肿瘤的发生,可能是肿瘤发生、侵袭和增殖的重要途径之一.

Expression of p-p38MAPK, uPA and Ki-67 in epithelial odontogenic tumour

Objective To examine the expression of phosphorylated p38 mitogen-activated protein kinase (p-p38MAPK) , urokinase plasminogen activator (uPA) and Ki-67. Methods The specimens of ameloblastoma (AB) , keratocystic odontogenic tumour (KCOT) , calcifying epithelial odontogenic tumor (CEOT), adenomatoid odontogenic tumour (AOT) , calcifying cystic odontogenic tumour (CCOT) and 5 tooth germs were examined immunohistochemically for the expression of p-p38MAPK, uPA and Ki-67. Results p-p38MAPK was detected both in the cytoplasm and the nucleus of the epithelial odontogenic tumour cells and uPA in the cytoplasm of the epithelial odontogenic tumour cells. Among the 65 cases, there were 17(26%) ,51 (78%) and 62 cases(95%) of positive expression of p-p38MAPK, uPA and Ki-67 protein respectively. Furthermore, there was a statistically significant difference in the expression of p-p38MAPK, uPA and Ki-67 between epithelial odontogenic tumor group and tooth germ group(P <0. 05). There were significant correlations among the expression of p-p38MAPK, uPA and Ki-67 (P < 0.05). Conclusions The p38MAPK-signaling pathway could promote tumour growth and invasion in epithelial odontogenic tumour by up-regulating uPA protein expression and may play a role in oncogenesis, invasion and proliferation of epithelial odontogenic tumour.