Transforming growth factor beta 1 and its receptor types I and II. Comparison in human normal prostate, benign prostatic hyperplasia, and prostatic carcinoma
M. Royuela et al., Transforming growth factor beta 1 and its receptor types I and II. Comparison in human normal prostate, benign prostatic hyperplasia, and prostatic carcinoma, GROW FACTOR, 16(2), 1998, pp. 101-110
An immunohistochemical and semiquantitative comparative study of transformi
ng growth factor beta 1 (TGF-beta 1) and its receptor types I (TGF-beta RI)
and II (TGF-beta RII) was carried out in normal prostates and in the prost
ates from men with benign prostatic hyperplasia (BPH), and men with prostat
ic adenocarcinoma. Immunoreaction to TGF-beta 1 was limited to the basal ep
ithelial cells in the normal prostates. Some cells in the connective tissue
stroma were also stained. In BPH immunolabelling was also observed in colu
mnar (secretory) cells of the epithelium. In prostatic adenocarcinoma, all
epithelial cell types were intensely immunostained. Some stromal cells were
also stained. Immunostaining to TGF-beta RI was only present in the basal
cells in normal prostates. In BPH, this immunoreaction was found in the who
le epithelium and in some stromal cells. In prostatic cancer, the immunosta
ining pattern for this receptor was similar to that of BPH but more intense
in the epithelial cells. Immunoreactivity to TGF-beta RII appeared in some
basal cells and some scattered columnar cells of the normal prostate epith
elium. In the BPH sections, this pattern was maintained, and a weak immunol
abelling was also observed in the stroma. In prostate cancer, all epithelia
l cells appeared intensely labelled. In the stroma, immunolabelling was sim
ilar to that of the BPH specimens. The results of the present study suggest
that, in normal prostates, only the basal cells of the epithelium posses b
oth receptor types, and hence can transduce TGF-beta 1 signal intracellular
ly. The basal cells can also secrete this growth factor which would act as
an autocrine inhibitory growth factor for them. In addition, TGF-beta 1 is
secreted in some zones by stromal cells, acting then as a paracrine growth
factor for basal cells in those areas. In BPH, in addition to the basal cel
ls, some secretory columnar cells also secrete TGF-beta 1 and possess both
types of TGF-beta 1 receptors, and thus, both epithelial cell types are sus
ceptible to TGF-beta 1 action. Since both receptor types are also present i
n some stromal cells, these cells also perform an autocrine secretion, in a
ddition to their paracrine secretion to the epithelial cells. TGF-beta RIIs
seem to be more numerous than TGF-beta RIs and this lead us to hypothesize
that these incomplete receptors might be a protection against the inhibiti
on caused by TGF-beta 1 action. In prostatic carcinoma all cell types displ
ay the same characteristics as in BPH, although both receptor types are fou
nd in similar numbers, and thus, the above mentioned protection would not o
ccur.