The aim of this study was to investigate the effect of cell spreading
on the induction of ornithine decarboxylase and the rate of putrescine
uptake in anchorage-dependent and anchorage-independent cells. Platin
g non-transformed IEC-6 epithelial cells at high versus low cell densi
ty restricted cell spreading from 900 mu m(2) to approximately 140 mu
m(2), blunted the transient induction of ornithine decarboxylase activ
ity from 202 to 32 pmol (CO2)-C-14/mg protein per hour and reduced the
rate of [C-14]putrescine uptake from 46 to 23 pmol/10(5) cells per ho
ur, The mean spreading area of the cell population was controlled by c
oating tissue culture dishes with the nonadhesive polymer, polyHEMA, O
rnithine decarboxylase activity and putrescine uptake correlated with
cell spreading with minimal spreading (263 mu m(2)) corresponding to a
n 83% decrease in ornithine decarboxylase activity and 51% decrease in
the rate of putrescine uptake, Adding the RGD peptide, Gly-Arg-Gly-Gl
u-Ser-Pro to the medium of sparsely plated cells resulted in rapid red
uctions in cell spreading concomitant with dose-dependent decreases in
ornithine decarboxylase activity and putrescine uptake, Finally, mini
mizing cell spreading by depriving cells of substratum contact complet
ely abolished serum-induced increases in ornithine decarboxylase and r
educed the rate of putrescine uptake by 47%. In contrast to IEC-6 cell
s, ornithine decarboxylase of neoplastic HTC-116 cells was constitutiv
ely expressed with basal and stimulated activity (193 and 982 pmol (CO
2)-C-14/mg protein per hour, respectively) completely independent of c
ell adhesion, Putrescine uptake, however, was abolished in the absence
of cell adhesion, These data suggest that the induction of ornithine
decarboxylase activity and the rate of putrescine uptake correlate wit
h spreading of anchorage-dependent IEC-6 cells and that ornithine deca
rboxylase activity, but not putrescine uptake, appears to be independe
nt of spreading of neoplastic HTC-116 cells.