Carcinogenesis, Vol 18, 715-719, Copyright © 1997 by Oxford University Press
CA La Porta, L Tessitore and R Comolli
PKC, a family of 11 related isoforms, appears deeply implicated in
carcinogenesis and in the metastatic process, however, little being known
on the specific role of each isoform in that process. In this work we
analysed the subcellular distribution and the in situ expression of
classical PKC (alpha and beta) isoforms and the expression of PKC delta in
the tumour and lung-metastases induced in the rat using the 'resistant
hepatocyte' model of diethylnitrosamine- induced hepatocarcinogenesis. With
respect to control untreated liver, an activation and increased expression
of PKC alpha was observed in tumour and lung metastatic nodules, while
cytosolic and membrane PKC beta was undetectable. In contrast, nuclear PKC
beta showed an increased activity in the tumour and a marked increased
activity and expression in metastatic nodules, suggesting a possible role
of such isoform in the metastatic process. The analysis of PKC delta
expression revealed a down regulation in both tissues with respect to
control untreated liver, suggesting the inhibitory role of such isoform on
tumour cell proliferation in agreement with our previous observations.
Taken together, these results point to a different role for PKC alpha and
delta in the development of tumour and metastatic nodules using the
'resistant hepatocyte' model of liver carcinogenesis, and suggest a
possible involvement of nuclear PKC beta in the development of secondary
tumours.
ARTICLES
Changes in protein kinase C alpha, delta and in nuclear beta isoform expression in tumour and lung metastatic nodules induced by diethylnitrosamine in the rat
Department of General Physiology and Biochemistry, University of Milan, Italy.
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