【作者】 金卉；

【导师】 黄杰安；

【作者基本信息】 广西医科大学 ， 消化内科， 2010， 硕士

【摘要】 目的：检测鞘氨醇激酶1(SphK1)及1-磷酸鞘氨醇(S1P)受体(S1P1,2,3)在正常大肠组织、大肠腺瘤、大肠腺癌、伴有远处转移的大肠腺癌组织中的表达情况,探讨SphK1/S1P通路在大肠癌发生发展中的可能作用及其临床意义。方法：收集人大肠腺癌组织标本24例、大肠腺瘤组织标本12例、正常大肠组织标本12例。应用RT-PCR方法检测各组织标本中SphK1与S1P1,2,3 mRNA表达水平。应用Western Blot方法检测各组织标本SphK1与1-磷酸鞘氨醇受体1(S1P1)的蛋白表达。结果：SphKl mRNA、SI P1 mRNA1 S1P2mRNA1 S1P3mRNA的表达在伴有远处转移的大肠腺癌组织、无远处转移的大肠腺癌、大肠腺瘤、正常大肠组织呈依次递减趋势,各组间比较均有显著的统计学差异(p<0.01)。与此相似,SphK1与S1P1蛋白在各组中的表达亦与其mRNA表达一致,呈现从高到低表达的趋势。大肠腺癌SphK1 mRNA表达量的多少与患者的年龄、性别、部位无关,而与浸润深度及淋巴结转移有关。结论：SphKl及其底物的受体表达异常可能参与了大肠肿瘤的发生发展。更多还原

【Abstract】 Objective:Analyze the expression of sphingosine kinases 1(SphKl) and sphingosine-1-phosphate (SIP) receptors (SIP1,2,3) in tissues of normal colon, colorectal adenoma, colorectal adenocarcinoma, colorectal adenocarcinoma with distant metastasis and approach the possible role of SphK/S1P pathway in colorectal cancer development and progression and its clinical significance.Methods:Randomly collect 12 normal colon tissues,12 colorectal adenoma tissues,12 colorectal adenocarcinoma tissues and 12 tissues of colorectal adenocarcinoma with distant metastasis. The expressions of SphKl, S1P1, S1P2, S1P3 mRNA in tissues were detected by RT-PCR. The protein expressions of SphKl, S1 P1 were evaluated by Western blot.Results:The expression of SphKl, S1P1, S1P2, S1P3 mRNA in colorectal adenocarcinoma with distant metastasis group, colorectal adenocarcinoma group, colorectal adenoma group, normal colon group is showed a decreasing trend in turn, and between groups the differences were significantly. Similarly, the protein expressions of SphK1, S1P1 in the 4 groups are consistent with their mRNA expression, showed a trend from high to low. The expression of SphKl mRNA is associated with the depth of invasion and the level of lymph node metastasis, while it is unrelated with patient’s age, sex and the location of colorectal adenocarcinoma.Conclusions:The abnormal expression of SphK1 and S1P receptors may be involved in colorectal tumor occurrence and development.更多还原