survivin基因表达与非小细胞肺癌发生发展的关系

Expression of survivin gene and its significance in the carcinogenesis and development of non-small cell lung cancer

目的 研究非小细胞肺癌 (NSCLC)组织中survivinmRNA的表达 ,探讨其在NSCLC发生发展、浸润转移中的作用。方法 原位杂交法检测 12例正常支气管粘膜上皮、9例不典型增生、3 4例NSCLC、12例淋巴结转移癌组织中survivinmRNA的表达。结果 在正常支气管粘膜上皮、不典型增生、肺癌及淋巴结转移癌组织中survivinmRNA阳性表达率呈递增趋势 ,分别为 16.67% ( 2 /12 )、3 3 .3 3 % ( 3 /9)、61.76% ( 2 1/3 4)、91.67% ( 11/12 ) ,其中肺癌、淋巴结转移癌组织阳性表达率与正常支气管粘膜上皮比较 ,差异均有显著性 (P<0 .0 1,P <0 .0 1)。低分化肺癌survivinmRNA阳性表达率 88.89% ( 8/9)和中分化肺癌 75 .0 0 % ( 12 /16)均显著高于高分化肺癌 11.11% ( 1/9) (P =0 .0 0 3 ,P =0 .0 0 4)。survivin基因表达与NSCLC组织学类型及有无淋巴结转移无明显关系 (P >0 .0 5 ,P >0 .0 5 )。结论 survivin基因可能在肺癌的发生发展中起着重要作用 ;封闭或下调survivin基因的表达水平 ,恢复正常凋亡调控机制 。

Objective To study the expression of survivin mRNA in non small cell lung cancer (NSCLC), and to explore its relationship with carcinogenesis, development invasion and metastasis of NSCLC. Methods In situ hybridization was applied to detect survivin mRNA expression in 12 normal bronchial epithelium, 9 dysplasia, 34 NSCLC and 12 metastatic lymph nodes. The relationship between survivin expression and clinicopathological characteristics was analyzed. Results In normal bronchial epithelium, dysplasia, NSCLC and metastatic lymph nodes, the positive rate of survivin mRNA expression were 16.67% (2/12), 33.33% (3/9), 61.76% (21/34), and 91.67% (11/12), respectively. There were significant differences in survivin mRNA expression between lung cancer and normal bronchial epithelium ( P <0.01), as well as between metastatic lymph nodes and normal bronchial epithelium ( P <0.001). There were remarkably higher survivin mRNA expressions in poor and moderate differentiated groups than that in well differentiated group ( P =0.003, P =0.004). The expression of survivin mRNA was not related to histologic classification and lymph node status ( P >0.05, P >0.05). Conclusion Survivin mRNA expression may play an important role in the carcinogenesis and development of NSCLC. It may be a new target in gene therapy of lung cancer through blocking or down regulating survivin mRNA expression to recover the normal regulation mechanism of apoptosis.