EXPRESSION OF 32 67-KDA LAMININ RECEPTOR IN LAMININ ADHESION-SELECTEDHUMAN COLON-CANCER CELL-LINES/

Citation
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
Citations number
28
Categorie Soggetti
Oncology
Journal title
ISSN journal
00070920
Volume
77
Issue
1
Year of publication
1998
Pages
15 - 20
Database
ISI
SICI code
0007-0920(1998)77:1<15:EO36LR>2.0.ZU;2-S
Abstract
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.