IN-VITRO INFLUENCE OF PHASEOLUS-VULGARIS, GRIFFONIA-SIMPLICIFOLIA, CONCANAVALIN-A, WHEAT-GERM, AND PEANUT AGGLUTININS ON HCT-15, LOVO, AND SW837 HUMAN COLORECTAL-CANCER CELL-GROWTH
R. Kiss et al., IN-VITRO INFLUENCE OF PHASEOLUS-VULGARIS, GRIFFONIA-SIMPLICIFOLIA, CONCANAVALIN-A, WHEAT-GERM, AND PEANUT AGGLUTININS ON HCT-15, LOVO, AND SW837 HUMAN COLORECTAL-CANCER CELL-GROWTH, Gut, 40(2), 1997, pp. 253-261
Background/Aims-Compared with normal colonic mucosa, lectin receptor e
xpression is increased in hyperplastic and neoplastic tissues; some le
ctins have been shown to influence human colonic epithelial cell proli
feration. The aim was to assess further the influence lectins (Phaseol
us vulgaris Griffonia simplicifolia (GSA), concanavalin A (Con A), whe
at germ (WGA), and peanut (PHA-L) agglutinins) on cellular growth in t
hree human colorectal cancer cell lines (LoVo, HCT-15 and SW837). Meth
ods-Cells were cultured in four lectin concenrations (0.1, 1.0, 10, an
d 100 mu g/ml) and growth assessed at days 2, 3, 5, and 7. The experim
ents were performed in media supplemented with either 1% or 10% fetal
calf serum (FCS). Growth was assessed using the MTT (3-(4,5)-dimethylt
hiazol-2-yl)-2,5-diphenyl tetrazolium bromide) colorimetric assay. Res
ults-Growth in each cell line was greatly affected by at least two of
the lectins tested. There was some variation in the effect of a given
lectin on different cell lines. Lectin effects showed a dose-response
and the greatest effects generally resulted from the highest concenrat
ions at the longest culture time. WGA and Con A induced large effects
in all cell lines; the effects of Con A were partly blocked by the hig
her concentration of FCS. PNA had modest and uniform stimulatory effec
ts overall. The effects of GSA and PHA-L varied between cell lines. Co
nclusions-The lectins studied all have the potential to affect colonic
cancer growth in vitro. Many dietary lectins are resistant to digesti
on and may have important effects in vitro but the definition of their
role in human colonic cancer biology must take into account the varia
bility in lectin response.