着丝粒蛋白A在原发性肝癌中的表达

Expression of centromere protein A in hepatocellular carcinoma

目的研究乙肝病毒X蛋白（HBx）上调的基因着丝粒蛋白A（centromere protein A，CENP-A）在原发性肝细胞癌（HCC）及癌旁组织的表达差异，并初步探讨其意义。方法应用RT-PCR和即时定量PCR（real-time quantitative PCR）方法，检测20例HCC及配对癌旁肝组织中CENP-A基因mRNA的表达水平，应用免疫组织化学方法检测80例HCC和癌旁肝组织中CENP-A蛋白、p53蛋白的表达情况。结果CENP-A mRNA在癌及癌旁组织中的相对表达水平分别为（0．64±0．18）和（0．09±0．09），二者差异有统计学意义（t=12．78，P〈0．01）。免疫组织化学结果显示：CENP-A在HCC组织中的总阳性率为71．25％（57／80），高于配对癌旁组织的总阳性率43．75％（35／80）（x^2=12．38，P〈0．01）。p53在癌组织中的总阳性率为75％（60／80），高于配对癌旁组织中的总阳性率16．25％（13／80）（x^2=55．65，P〈0．01），p53与CENP-A在癌组织中的表达一致性达88．75％（71／80），呈正相关（r=0．57，P〈0．01）。结论CENP-A在肝癌组织中的过表达与细胞恶性增殖相关，且这种过表达是由转录水平引起的，其机制可能与p53基因的转录调节有关。

Objective To study the expression of centromere protein A （CENP-A） and its significance in hepatocellular carcinoma （HCC） and adjacent non-neoplastic hver tissue. Methods The expression levels of CENP-A mRNA in 20 samples of HCC and adjacent non-neoplastic liver tissue were analyzed by reverse transcription-polymerase chain reaction （RT-PCR） and real-time quantitative polymerase chain reaction （qRT-PCR）. Immunohistochemical study for CENP-A and p53 proteins was also performed on tissue microarrays containing 80 samples of HCC and adjacent liver tissue. Results The expression level of CENP-A mRNA in HCC （0. 64 ± 0. 18 ） was higher than that in adjacent non-neoplastic liver tissue （0.09±0.09） （t = 12.78, P〈0.01）. Of the 80 samples of HCC, 57 cases （71.25%） and 60 cases （75%） expressed CENP-A and p.53 proteins respectively. The positivity rates of CENP-A and p.53 proteins in non-neoplastic liver tissue were 43.75% （35/80） and 16.25% （13/80） respectively. There was a statistically significant difference in CENP-A and p.53 protein expression between HCC and non-neoplastic liver tissue （P 〈0. 01 ）. The coincident rate between CENP-A and p.53 expression was 88. 75% （71/80）. Expression of CENP-A protein showed a positive correlation with that of p.53 protein （ r = 0. 57, P 〈 0. 01 ）. Conclusion The over-expression of CENP-A occurs at transcriptional level and may be related to malignant proliferation of HCC via possible interaction with p53 gene.