Open AccessLack 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)
Author(s) -
Mesnil Marc,
Piccoli Colette,
Klein JeanLouis,
Morand Isabelle,
Yamasaki Hiroshi
Publication year - 1993
Publication title -
japanese journal of cancer research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.035
H-Index - 141
eISSN - 1349-7006
pISSN - 0910-5050
DOI - 10.1111/j.1349-7006.1993.tb02038.x
Subject(s) - cell adhesion molecule , cadherin , biology , deleted in colorectal cancer , cell adhesion , microbiology and biotechnology , carcinogenesis , cell culture , cell , cell–cell interaction , colorectal cancer , gene , gene expression , neural cell adhesion molecule , phenotype , cancer research , cancer , genetics
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.