NSCLC中Kai1和FasL表达及其临床病理意义

Expression of Kai1 and FasL in non-small cell lung cancer and its clinicopathological significance

背景与目的Kai1属四跨膜超家族成员,参与细胞增殖、粘附和运动的调节,其表达下调与肿瘤进展和预后关系密切。Fas配体(FasL)是肿瘤坏死因子受体/神经生长因子家族成员,可激活在细胞凋亡中起关键作用的caspase3,并可导致肿瘤细胞的免疫逃逸。本研究拟观察Kai1和FasL在非小细胞肺癌(NSCLC)中的表达,探讨其在NSCLC发生和进展中的作用及相互关系。方法采用SP免疫组化方法检测Kai1和FasL在NSCLC及癌旁正常肺组织中的表达,比较其表达与患者临床病理特征的关系,分析NSCLC中Kai1和FasL表达的相互关系。结果79例NSCLC中Kai1表达阳性率显著低于癌旁正常肺组织(55.7%比82.6%,P<0.05),NSCLC中FasL阳性表达率高于癌旁正常组织(73.4%比52.2%,P<0.05)。Kai1蛋白表达与患者年龄、性别、肿瘤部位和组织学分型无关(P>0.05),与淋巴结转移和临床病理分期呈负相关(P<0.05),与组织分级呈正相关(P<0.05)。FasL蛋白表达与患者年龄、性别、肿瘤部位和组织学分型无关(P>0.05),与淋巴结转移呈正相关(P<0.05),与组织分级成负相关(P<0.05)。NSCLC中Kai1和FasL蛋白表达密切相关(P<0.05)。结论Kai1表达下调和FasL表达上调在NSCLC发展中起重要作用。它们有望成为反映NSCLC进展的分子生物学指标。NSCLC中FasL和Kai1表达密切相关,为FasL调节NSCLC中Kai1表达提供了新的实验依据。

Background and objective It has been known that Kail is one of transmembrane 4 superfamily regulating cell proliferation, adhesion and mobility and its down-regulated expression is closely correlated with progression and prognosis of tumor. Fas ligand （FasID is one of tumor necrosis factor/nerve growth factor family activating caspase-3, a key proteinase in cell apoptosis and leading immune escape in tumor cells. The aim of this study is to investigate the expression of Kail and FasL in non-small cell lung cancer （NSCLC） and to explore their roles and relationship in carcinogenesis and progression of NSCLC. Methods Kail and FasI. expressions were examined in 79 NSCLC tissues and their adjacent normal lung tissues by SP immunohistochemistry. Their expressions were compared with clinicopathological features of NSCI.C. The relationship between Kail and FasL expressions was also analyzed in NSCI.C. Results Kail expression in NSCLC tissue was remarkably lower than thai in their adjacent tissue （55.7%vs 82.6%, P〈0.05）. However, it was the converse for FasL （73.4% vs 52.2%, P〈0.05）. Kail expression was not correlated with age and gender of NSCLC patients, tumor location or histological classification （P〉0.05）, but negatively with lymph node metastasis and clinicopathological staging and positively with differentiation degree （P〈0.05）. FasL expression was not correlated with age and gender of the patients, tumor location or histological classification （P〉0.05）, but positively with lymph node metastasis and negatively with differentiation degree （P〈0.05）. Kail expres sion was closely correlated with FasL expression in NSCLC （P〈0.05）. Conclusion Down regulation of Kail expression and up-regulation of FasL may play important roles in carcinogenesis and progression of NSCLC. Kail and FasL could be considered as molecular markers to reflect pathobiological behavior of NSCLC. Additionally, close correlation of FasL expression with Kail expression in NSCI.C provides a novel insight into the regulatory effects of FasI. expression on Kail expression.