论文部分内容阅读
目的:探讨SYK(Spleentyrosinekinase,脾酪氨酸激酶)在肝细胞癌中的表达和不表达的机制。方法:分别用逆转录-聚合酶链反应(RT-PCR)方法和甲基化特异性聚合酶链反应(Methylation-specificPCR,MSP)检测SYK基因在肝癌细胞系(HepG2和Hep3B)和34例肝细胞癌组织、癌旁非瘤组织中的表达和甲基化情况。结果:肝癌细胞系Hep3B表达SYKmRNA,而HepG2不表达SYKmRNA。DNA甲基化转移酶抑制剂5-aza-2’-deoxycytidine处理HepG2后,SYK重新表达。Hep3B细胞SYK甲基化阴性,HepG2细胞SYK甲基化阳性。34例肝细胞癌组织标本中,5例SYKmRNA表达阴性,SYK基因甲基化均阳性;29例SYKmRNA表达阳性,其中3例SYK甲基化阳性,其余26例SYK甲基化阴性。肿瘤组织SYK基因的甲基化率为23.5%(8/34),而瘤旁肝组织中为8.8%(3/34)。结论:SYK基因启动子甲基化导致肝细胞癌SYKmRNA失表达,可能是肝癌发病的机制之一。
Objective: To investigate the mechanism of SYK (Spleentyrosinekinase, spleen tyrosine kinase) expression and non-expression in hepatocellular carcinoma. Methods: SYK gene was detected by reverse transcription polymerase chain reaction (RT-PCR) and Methylation-specific PCR (MSP) in hepatoma cell lines (HepG2 and Hep3B) Cell carcinoma, adjacent non-cancerous tissue expression and methylation. Results: Hep3B cells expressed SYK mRNA while HepG2 cells did not express SYK mRNA. After HepG2 was treated with 5-aza-2’-deoxycytidine, a DNA methyltransferase inhibitor, SYK was re-expressed. SYK methylation of Hep3B cells was negative, and SYK methylation of HepG2 cells was positive. Among 34 hepatocellular carcinoma samples, 5 cases showed negative SYK mRNA expression and SYK gene methylation were positive, 29 cases expressed positive SYK mRNA, 3 cases were positive for SYK methylation and 26 cases were negative for SYK methylation. The methylation rate of SYK gene in tumor tissue was 23.5% (8/34), while it was 8.8% (3/34) in para-tumor liver tissue. Conclusion: SYK gene promoter methylation causes loss of expression of SYK mRNA in hepatocellular carcinoma, which may be one of the mechanisms of hepatocellular carcinoma.