Mi. Arenas et al., E-, N- and P-cadherin, and alpha-, beta- and gamma-catenin protein expression in normal, hyperplastic and carcinomatous human prostate, HISTOCHEM J, 32(11), 2000, pp. 659-667
The expression of E-, N- and P-cadherin, alpha-, beta- and gamma -catenin,
and actin was studied by immunohistochemistry, ELISA, and Western blot anal
ysis in normal prostates, and in the prostates of men with benign prostatic
hyperplasia and men with prostatic carcinoma, in order to evaluate their p
ossible role in the pathogenesis of these diseases. Present results reveal
that the immunophenotype of hyperplastic prostates differs from those of bo
th normal and carcinomatous prostates in the intracellular distribution (ob
served by immunohistochemistry) and the intensity (measured by ELISA) of im
munoreactions to cadherins, catenins, and actin. Hyperplastic prostates dif
fer form normal prostates in the weaker immunoreaction to the three cadheri
n types, the two catenins, and actin, as well as in the intracellular distr
ibution of P-cadherin, beta- and gamma -catenin, and actin. Differences bet
ween benign prostatic hyperplasia and prostatic carcinoma are less marked b
ecause hyperplastic prostates differ from carcinomatous prostates only in t
he weaker immunoreactions to P-cadherin, and alpha -catenin. The most remar
kable findings in this study were: (1) alpha -catenin production was elevat
ed in prostatic carcinoma in comparison with benign prostatic hyperplasia a
nd normal prostate; and (2) P-cadherin expression in benign prostatic hyper
plasia is reduced with regard to those of normal and carcinomatous prostate
s. It may be concluded that a decreased immunoreaction to cadherins, cateni
ns, and actin, as well as changes in the intracellular distribution of acti
n in prostatic cells are not necessarily suggestive of malignancy, because
these alterations are also present in BPH, and thus, the loss of cadherin-c
atenin-mediated adhesion alone is not sufficient to establish an invasive p
henotype.