在肝癌发生早期阶段，RUNX1、RUNX3和CBFβ在肝细胞癌中的表达下调。
Down-regulation of RUNX1, RUNX3 and CBFbeta in hepatocellular carcinomas in an early stage of hepatocarcinogenesis.
作者信息
Miyagawa Kouji, Sakakura Chouhei, Nakashima Susumu, Yoshikawa Tetsuji, Kin Shuichi, Nakase Yuenn, Ito Kosei, Yamagishi Hisakazu, Ida Hiroshi, Yazumi Shujiro, Chiba Tsutomu, Ito Yoshiaki, Hagiwara Akeo
机构信息
Department of Surgery and Regenerative Medicine, Division of Surgery and Physiology of Digestive System, Kyoto Prefectural University of Medicine, Kamigyo-ku, Kawaramachi-dori, Kyoto 602-8566, Japan.
出版信息
Anticancer Res. 2006 Sep-Oct;26(5B):3633-43.
BACKGROUND
Our previous studies suggested that deficient function of RUNX3 protein is causally related to development and progression of human gastric cancer. RUNX3 is mapped to 1p36, which is frequently deleted in hepatocellular carcinomas (HCC), therefore, these tumors were investigated for expression and copy number changes of RUNX3 and other Runt-related genes, RUNX1, RUNX2, and their co-factor CBFP. Similarly nearby uninvolved liver showing cirrhosis or normal histology was investigated in conjunction with various clinicopathological factors.
MATERIALS AND METHODS
Copy number change and expression change of RUNX family genes in 35 hepatocellular carcinoma specimens and adjoining liver with cirrhosis (LC) or normal histology were estimated using quantitative reverse transcription polymerase chain reaction (RT-PCR) and in situ hybridization.
背景
我们之前的研究表明，RUNX3蛋白功能缺陷与人类胃癌的发生和发展存在因果关系。RUNX3定位于1p36，在肝细胞癌（HCC）中该区域常发生缺失，因此，对这些肿瘤中RUNX3以及其他与Runt相关的基因RUNX1、RUNX2及其辅因子CBFP的表达和拷贝数变化进行了研究。同样，对附近显示肝硬化或正常组织学的未受累肝脏，结合各种临床病理因素进行了研究。
材料与方法
使用定量逆转录聚合酶链反应（RT-PCR）和原位杂交技术，对35例肝细胞癌标本以及伴有肝硬化（LC）或正常组织学的相邻肝脏中RUNX家族基因的拷贝数变化和表达变化进行评估。
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