首页> 美国卫生研究院文献>Cancer Science >Lack of Correlation between the Gap Junctional Communication Capacity of Human Colon Cancer Cell Lines and Expression of the DCC Gene a Homologue of a Cell Adhesion Molecule (N‐CAM)
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Lack of Correlation between the Gap Junctional Communication Capacity of Human Colon Cancer Cell Lines and Expression of the DCC Gene a Homologue of a Cell Adhesion Molecule (N‐CAM)

机译:人类结肠癌细胞系的间隙连接沟通能力与DCC基因(细胞粘附分子的同系物)的表达之间缺乏相关性

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摘要

In many human colorectal cancers, the DCC gene encoding for a homologue of the neural cell adhesion molecule (N‐CAM) is found to be deleted. Previous work suggested that gap Junctional intercellular communication (GJIC) might play an important role in carcinogenesis and could be regulated by the expression of cell adhesion molecules such as E‐cadherin in some epithelial cell systems. In order to examine whether the deletion of the putative cell adhesion molecule DCC is related to the level of GJIC, which might, in turn, be important in human colorectal cancers, we compared levels of expression of the DCC gene with the GJIC capacity of a panel of human colorectal adenocarcinoma cell lines isolated from different stages of tumor progression. While the level of GJIC varied between the cell lines studied, we found no correlation between their communication capacity and DCC expression revealed by a reverse‐transcriptase/polymerase chain reaction method. This lack of correlation suggests that DCC is not a crucial regulator of GJIC.
机译:在许多人类大肠癌中,发现编码神经细胞粘附分子(N-CAM)同源物的DCC基因被删除。先前的研究表明,间隙连接细胞间通讯(GJIC)可能在致癌作用中起重要作用,并可能受某些上皮细胞系统中细胞黏附分子(例如E-钙黏着蛋白)的表达调控。为了检查推定的细胞粘附分子DCC的缺失是否与GJIC的水平有关,GJIC的水平又可能在人大肠癌中很重要,我们比较了DCC基因的表达水平与GJIC的GJIC能力。从肿瘤进展的不同阶段分离的人结肠直肠腺癌细胞系。虽然在研究的细胞系之间GJIC的水平各不相同,但我们发现它们的通讯能力与逆转录酶/聚合酶链反应方法揭示的DCC表达之间没有相关性。这种缺乏相关性表明DCC并不是GJIC的关键调节器。

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