Wh. Kim et al., EXPRESSION OF 32 67-KDA LAMININ RECEPTOR IN LAMININ ADHESION-SELECTEDHUMAN COLON-CANCER CELL-LINES/, British Journal of Cancer, 77(1), 1998, pp. 15-20
Laminin promotes the malignant phenotype, and the expression of certai
n laminin receptors is increased in malignancy. Previously, we demonst
rated that a laminin-adhesive subclone of a human colon cancer cell li
ne showed increased tumorigenicity in nude mice and increased affinity
of the beta(1), integrin for laminin relative to the laminin-non-adhe
sive subclone. The total amount of either beta(1), integrin protein or
mRNA did not increase. As levels of the 32/67-kDa laminin receptor (6
7LR) correlate with malignancy, we examined 67LR expression in the lam
inin adhesion-selected human colon cancer cells. The laminin-adhesive
subclone, which was more tumorigenic in both heterotopic and orthotopi
c locations than in a laminin-non-adhesive subclone, showed cell-surfa
ce membrane staining of 67LR, whereas the laminin-non-adhesive subclon
e showed cytoplasmic staining of 67LR. No difference in either the amo
unt of 67LR mRNA or the amount of protein was observed in the parental
cells than in the laminin-adhesive and non-adhesive subclones. When a
ssayed on a laminin affinity column, more 67LR molecules bound to the
column with cell extracts from the laminin-adhesive subclone than was
observed with the nonadhesive subclone. These findings suggest that th
e increased tumorigenicity of laminin adhesion-selected tumour cells m
ight be due to an alteration in the distribution and/or adhesiveness o
f multiple receptors including 67LR and beta(1), integrin.