Human carcinoembryonic antigen (CEA), a widely used tumor marker, and CEACA
M6 [formerly nonspecific cross-reacting antigen (NCA)] are up-regulated in
many types of human cancers, whereas family member CEACAM1 [formerly biliar
y glycoprotein (BCP)] is usually down-regulated, Deregulated overexpression
of CEA/CEACAM6 but not CEACAM1 can inhibit the differentiation and disrupt
the polarization and tissue architecture of man different types of cells.
In this report, we show that CEA and CEACAM6, but not CEACAM1, markedly inh
ibit the apoptosis of cells when deprived of their anchorage to the extrace
llular matrix, a process known as anoikis. By blocking: this tissue archite
cture surveillance mechanism, the architectural perturbation initiated by C
EA/CEACAM6 can thus be maintained.