Carcinogenesis, Vol 18, 479-484, Copyright © 1997 by Oxford University Press
PA Amstad, H Liu, M Ichimiya, IK Berezesky and BF Trump
Manganese superoxide dismutase (MnSOD) has been found to be depleted in a
variety of tumor cells as well as in in vitro transformed cell lines,
suggesting that MnSOD may function as an anticarcinogen by protecting the
cell from oxidant-induced carcinogenesis. The relationship between MnSOD
expression and tumor promotion was studied by transfection of a human MnSOD
cDNA into the promotable mouse epidermal cell line JB6 clone41. The effect
of MnSOD overexpression on the promotion-sensitive phenotype of JB6 cells
was assessed by measuring growth characteristics such as growth rate and
the ability to form colonies in soft agar. Compared with the parental and
vector-transfected (gpt) control cells, MnSOD-overexpressing cells had a
slower growth rate and their ability to form colonies in soft agar was
significantly decreased in response to 12-O-tetradecanoylphorbol-13-acetate
(TPA) treatment. Since the transformation-sensitive phenotype of JB6
clone41 cells is associated with increased expression of the transcription
factor AP-1, we compared c-jun and c-fos mRNA expression in
MnSOD-transfected and control JB6 cells. Overexpression of MnSOD led to a
significant decrease in c-jun and c-fos expression in response to treatment
with TPA or the oxidant promoter superoxide. These findings indicate that
the promotion- sensitive phenotype of JB6 clone41 cells can be reverted by
increasing MnSOD intracellularly. A possible mechanism is that elevated
MnSOD expression might change the intracellular redox state by altering the
balance of reactive oxygen species. This could lead to a modulation of TPA
and oxidant-induced signal transduction pathways controlling cell growth
and differentiation.
ARTICLES
Manganese superoxide dismutase expression inhibits soft agar growth in JB6 clone41 mouse epidermal cells
Department of Pathology, University of Maryland, Baltimore 21201, USA.
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