Overexpression of α(1,3)-fucosyltransferase VII is sufficient for the acquisition of lung colonization phenotype in human lung adenocarcinoma HAL-24Luc cells.

Metastatic human lung adenocarcinoma HAL-8Luc cells display an enhanced expression of α(1,3)-fucosyltransferases (α(1,3)-Fuc-Ts) compared with their non-metastatic counterpart HAL-24Luc cells. This correlates with an increased surface expression of Lewisx(Lex)- and Lewisa(Lea)-related molecules and an in vitro enhanced adhesive capacity to E-selectin-expressing endothelial cells (Martin-Satué et al (1998). Cancer Res: 1544–1550). In the present work we have stably transfected HAL-24Luc cells with the cDNAs for the α(1,3)-Fuc-TIV and VII enzymes and analysed by flow cytometry the expression of Lex, sialyl-Lex, sialyl-Lexdimeric, Leaand sialyl-Lea. Fuc-TVII transfectants exclusively overexpress sialyl-Lexwhile Fuc-TIV-transfected cells only overexpress the Lexoligosaccharide. We show that solely Fuc-TVII transfectants are able to adhere to interleukin-1β-stimulated HUVEC monolayers. We also demonstrate that Fuc-TVII overexpression in HAL-24Luc cells is sufficient for the acquisition of the lung colonization phenotype. This is the first report directly showing the contribution of an α(1,3)-Fuc-T to the metastatic behaviour of human lung adenocarcinoma cells. [ABSTRACT FROM AUTHOR]