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目的:探讨Plk1在原发性肝细胞性肝癌中的表达及其意义。方法:用半定量RT-PCR、Western blot的方法检测21例原发性肝细胞性肝癌中Plk1的表达情况,并分析其与肝癌临床病理因素的关系。同时取肝硬化及正常肝组织各7例做对照。结果:肝癌组织中Plk1mRNA表达比值(Plk1/β-actin)为0.572±0.144,明显高于肝硬化组织中的0.250±0.057和正常肝组织的0.218±0.073(P<0.01)。Plk1 mRNA表达水平在肿瘤直径大于5 cm组中为0.641±0.110,而在肿瘤直径小于5 cm组中为0.458±0.120,两组之间比较有统计学差异(P<0.01)。其在有门静脉癌栓患者中的表达为0.652±0.107,明显高于无门静脉癌栓者中的表达0.522±0.144(P<0.05)。而与有无包膜,肿瘤病理分级和AFP阳性与否无明显相关。肝癌组织Plk1蛋白表达明显高于肝硬化及正常肝组织中的Plk1蛋白表达量。结论:原发性肝癌组织中Plk1mRNA及蛋白表达均明显增加;Plk1的表达高低与原发性肝癌的肿瘤直径大小及脉管侵犯有明显相关,提示其在肝癌生长及侵袭中发挥重要作用,为进一步研究肝癌的生长侵袭机制提供了思路。
Objective: To investigate the expression of Plk1 in primary hepatocellular carcinoma and its significance. Methods: The expression of Plk1 in 21 primary hepatocellular carcinoma was detected by semi-quantitative RT-PCR and Western blot. The relationship between Plk1 and clinical and pathological factors was analyzed. At the same time take cirrhosis and normal liver tissue in each of 7 cases as a control. Results: The Plk1 / β-actin expression in hepatocellular carcinoma was 0.572 ± 0.144, significantly higher than that in cirrhosis tissues (0.250 ± 0.057) and normal liver tissues (0.218 ± 0.073, P <0.01). The Plk1 mRNA expression level was 0.641 ± 0.110 in tumors with a diameter larger than 5 cm, and 0.458 ± 0.120 in tumors with a diameter less than 5 cm. The difference was statistically significant (P <0.01). Its expression in patients with portal vein tumor thrombus was 0.652 ± 0.107, which was significantly higher than that in patients without portal vein tumor embolus (0.522 ± 0.144, P <0.05). With or without capsule, tumor pathological grading and AFP positive or not no significant correlation. Plk1 protein expression in hepatocellular carcinoma was significantly higher than that in cirrhosis and normal liver tissues. Conclusion: The expression of Plk1 mRNA and protein were significantly increased in primary hepatocellular carcinoma. The expression of Plk1 was significantly correlated with tumor diameter and vascular invasion in primary hepatocellular carcinoma, suggesting that Plk1 plays an important role in the growth and invasion of hepatocellular carcinoma. Further study of the mechanism of growth and invasion of liver cancer provides a train of thought.