M. Mesnil et al., POSSIBLE MOLECULAR MECHANISM OF LOSS OF HOMOLOGOUS AND HETEROLOGOUS GAP JUNCTIONAL INTERCELLULAR COMMUNICATION IN RAT-LIVER EPITHELIAL-CELLLINES, Cell adhesion and communication, 2(5), 1994, pp. 377-384
We have previously characterized a series of rat liver epithelial cell
lines that exhibit levels of gap junctional intercellular communicati
on (GJIC) which are inversely related to their levels of expression of
transformed phenotypes. Cells of the non-tumorigenic line do not comm
unicate with their tumorigenic counterparts. We have examined the mole
cular mechanisms involved in this loss of homologous and heterologous
GJIC, employing a nontumorigenic cell line, IAR 20, and a tumorigenic
cell line, IAR 6-1. While both cell lines expressed a transcript codin
g for the gap junction protein, connexin 43 (ex 43), and similar level
s of ex 43 protein, they exhibited different phosphorylation states of
this protein, revealed by Western analysis. Immunohistochemical analy
sis showed that the nontumorigenic IAR 20 cell line, but not the tumor
igenic IAR 6-1 cells, was able to incorporate ex 43 gap junction plaqu
es extensively into their plasma membranes. When IAR 20 and LAR 6-1 ce
lls were co-cultured, ex 43 proteins were abundant in IAR 20 cells but
IAR 20/IAR 20 cell boundaries were ex 43-positive, while IAR 20/IAR 6
-1 boundaries were negative. The different phosphorylation state of oc
43 may partially explain the low GJIC of the IAR 6-1 cells and inabil
ity to communicate with their non-tumorigenic counterparts, but other
mechanisms such as cell-cell recognition processes may also be involve
d.