Chemistry Reference
In-Depth Information
Figure 25.2
Illustration of lectin - binding prop-
erties of tumor suppressor-negative (Mock)
and tumor suppressor-expressing (p16
INK4a
)
pancreatic carcinoma cells (Capan-1) by cytofl u-
orimetric analysis. Quantitative data on per-
centage of positive cells and fl uorescence inten-
sity are given in each panel. The gray area
represents the control in the absence of lectin,
the gray line represents carbohydrate-depen-
dent staining without removal of cell surface
sialic acids by sialidase and the black line rep-
resents staining after enzymatic desialylation.
The growth regulator galectin- 1 (Gal - 1) and the
plant lectin
Sambucus nigra
agglutinin (SNA)
recognizing
2,6 - sialylated Gal/GalNAc epit-
opes were used as probes.
α
monomeric galectin-3, teaches the lessons that binding and ensuing cross-
linking are required for the biological effect, and that functional antagonism
among members of a lectin family is operative (Figure 25.1 ) [11] . That lectin
pathways of growth regulation can be activated by master regulators of tumor
growth, especially a tumor suppressor, is illustrated in the next paragraph.
b) Loss of integrity of the tumor suppressor p16
INK4a
is observed frequently in
pancreatic cancer. In a model of human pancreatic carcinoma cells (Capan- 1)
the restoration of suppressor activity renders the cells susceptible to enter
programmed cell death when detached from a matrix (anoikis). Figure 25.2
presents a clue that the activity of this suppressor encompasses an effect on
cell surface glycosylation: the cell- staining profi les obtained with labeled human
lectin revealed that suppressor-positive cells are strongly reactive with galectin-
1, whereas control cells (Mock) must be subjected to a prior desialylation step
to acquire reactivity. The differing extent of sialylation is documented using a
plant lectin (
Sambucus nigra
agglutinin; for details on its sugar specifi city,
