Janssen-Timmen U, Traub O, Dermietzel R, Rabes H M, Willecke K
Carcinogenesis. 1986 Sep;7(9):1475-82. doi: 10.1093/carcin/7.9.1475.
A new rat monoclonal antibody was characterized which recognized the 26K protein in gap junctions of mouse, rat and human liver as shown by immunoblot, indirect immunofluorescence, and immunogold electron microscopy. This monoclonal antibody was used to investigate the abundance of gap junctions in chemically induced rat hepatocarcinomas. In comparison with livers of control animals we found in hepatocarcinomas an average decrease of 71% in the number of gap junctional immunofluorescent spots. A corresponding decrease of the total amount of the 26 K protein was detected by quantitative immunoblot. Changes in the proliferative state as well as in intercellular adhesion of hepatocarcinoma cells in contrast to normal hepatocytes might have contributed to cause this decrease of gap junctions in tumor tissue. Possibly the partial loss of gap junctions provided a selective advantage for those preneoplastic liver cells which developed into rapidly proliferating tumor cells.
一种新的大鼠单克隆抗体得到了鉴定，通过免疫印迹、间接免疫荧光和免疫金电子显微镜观察发现，该抗体可识别小鼠、大鼠和人肝脏间隙连接中的26K蛋白。此单克隆抗体用于研究化学诱导的大鼠肝癌中间隙连接的丰度。与对照动物的肝脏相比，我们发现肝癌中间隙连接免疫荧光斑点的数量平均减少了71%。通过定量免疫印迹检测到26K蛋白总量相应减少。与正常肝细胞相比，肝癌细胞增殖状态和细胞间黏附的变化可能导致了肿瘤组织中间隙连接的减少。间隙连接的部分丧失可能为那些发展成快速增殖肿瘤细胞的癌前肝细胞提供了选择性优势。
