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Glycobiology, Vol 9, 607-616, Copyright © 1999 by Oxford University Press
S Nishihara, T Hiraga, Y Ikehara, T Kudo, H Iwasaki, K Morozumi, S Akamatsu, T Tachikawa and H Narimatsu
Lewis b (Leb) antigens are gradiently expressed from the proximal to the
distal colon, i.e., they are abundantly expressed in the proximal colon,
but only faintly in the distal colon. In the distal colon, they begin to
increase at the adenoma stage of cancer development and then increase with
cancer progression. We aimed to clarify the molecular basis of Leb antigen
expression in correlation with the expression of other type I Lewis
antigens, such as Lewis a (Lea) and sialylated Lewis a (sLea), in colon
cancer cells. Considering the Se genotype and the relative activities of
the H and Se enzymes, the amounts of Leb antigens were proved to be
determined by both the H and Se enzymes in noncancerous and cancerous colon
tissues. But the Se enzyme made a much greater contribution to determining
the Lebamounts than the H enzyme. In noncancerous colons, the Se enzyme
were gradiently expressed in good correlation with the Leb expression,
while the H enzyme was constantly expressed throughout the whole colon. In
distal colon cancers, the H and Se enzymes were both significantly
upregulated in comparison with in adjacent noncancerous tissues. In
proximal colon cancers, expression of the H enzyme alone was highly
augmented. The augmented expression of Leb antigens in distal colon cancers
is caused mainly by upregulation of the Se enzyme and partly by the H
enzymes, while it is caused by upregulation of the H enzyme alone in
proximal colon cancers. The Se gene dosage profoundly influences the
amounts of the Leb, Lea, and sLea antigens in whole colon tissues,
regardless of whether they are noncancerous or cancerous tissues. It
suggests that the Se enzyme competes with alpha2,3 sialyltransferase(s) and
the Le enzyme for the type I acceptor substrates.
ORIGINAL ARTICLES
Molecular mechanisms of expression of Lewis b antigen and other type I Lewis antigens in human colorectal cancer
Division of Cell Biology, Institute of Life Science, Soka University, 1- 236 Tangi-cho, Hachioji, Tokyo 192-8577, Japan.
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