口腔鳞癌组织中Kai1基因、NF-kappaB/p50的表达及相关性研究

A Study of the Expressions and Correlation of Kai1 gene,NF-kappaB/p50 in Oral Squamous Cell Carcinoma

目的研究Kai1基因、NF-kappaB/p50在口腔鳞癌组织中的表达情况,分析二者在口腔鳞癌发生、发展进程中的作用及意义。方法运用免疫组织化学(SABC)法检测Kai1基因、NF-kappaB/p50在67例口腔鳞癌、28例淋巴结转移灶及23例口腔黏膜白斑、12例癌旁正常口腔黏膜组织中的表达。结果Kai1基因、NF-kappaB/p50的阳性表达率分别为:正常口腔黏膜100%、0%;口腔黏膜白斑(伴中、重度不典型性增生)86.9%、4.4%;无淋巴结转移的口腔鳞癌原发灶59.0%、12.8%;有淋巴结转移的口腔鳞癌原发灶28.6%、57.1%;淋巴结转移灶7.14%、82.1%。有转移的原发灶组较无转移组中Kai1基因的表达明显减低,而其在淋巴结转移灶中的表达又比相对应的原发灶组中的表达进一步减低,差异有统计学意义(χ2=6.0599,P=0.0138;χ2=4.3826,P=0.0363)。有淋巴结转移与无淋巴结转移的原发灶相比较,NF-kappaB/p50在细胞质、胞核中的表达明显增高(χ2=14.8787,P=0.0001);而其在淋巴结转移灶中的表达进一步增高(χ2=4.1388,P=0.0419)。Kai1/CD82、NF-kappaB/p50在口腔鳞癌中的表达呈明显的负相关性(r=-0.5345,P=0.0000)。二者在口腔鳞癌中的表达与患者的年龄、性别、病程、肿块的大小、癌组织浸润的深度、肿瘤的pTNM分期及组织分化程度等临床病理参数均无关(P>0.05)。结论Kai1基因表达下调、NF-kappaB的表达增高很可能促进了口腔鳞癌的转移,Kai1基因的表达减低可能与NF-kappaB的激活有关。

Objective To investigate the expressions of Kail , NF-kappaB/p50 in OSCC and their correlation. Methods The expressions of Kail/CD82 protein and NF-kappaB/p50 were detected by immunohistoehemistry （SABC） in a series of oral turnouts （39 primary OSCC without, 28 primary OSCC with lymph node metastases and 28 lymph node metastasis） , 23 oral leukoplasia and 12 normal oral squamous epithelia adjacent to turnouts. Results The positive rates of Kail gene expressions in normal, leukoplasias, primary OSCC without and with metastases and lymph node metastasis group were 100% （ 12/12）, 86.9% （20/23）, 59.0% （23/39）, 28.6% （8/28）and 7.14% （2/28） respectively, while NF-kappaB/p50 were 0% , 4.4% , 12.8% , 57.1% and 82.1% respectively. Kail gene expression, which in primary OSCC with metastasis group was lower than that in primary OSCC without metastasis group （Χ^2 = 6. 0599 ,P = 0. 0138 ） , reduced significantly even more in lymph node metastasis compared with correspondence primary locus （Χ^2 = 4. 3826, P = 0. 0363 ）. The expression of NF-kappaB/p50 was obviously higher in primary OSCC lesion with metastasis than that in primary lesion without metastasis （Χ^2 = 14. 8787,P = 0. 0001 ） , and it was even higher in lymph metastasis lesion （Χ^2 = 4. 1388 ,P = 0. 0419）. The down-regulated expressions of Kail gene was closely related to the activated expression of NF-kappaB/p50 in OSCC cells （ r = - 0. 5345, P = 0. 0000）. The expressions of Kail/CD82 and NF-kappaB/p50 were not statistically related with clinicopathological parameters of OSCC （ P 〉 0.05 ）. Conclusions The down-regulated expression of Kail gene and the aberrant high expression of NF-kappaB/p50 might prompt OSCC metastasis. Kail gene may be one of mediators for NF-kappaB to regulate OSCC metastasis.