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J Biol Chem, Vol. 274, Issue 21, 14595-14601, May 21, 1999
From The Hormel Institute, University of Minnesota,
Austin, Minnesota 55912
Trivalent arsenic (arsenite,
As3+) is a human carcinogen, which is associated with
cancers of skin, lung, liver, and bladder. However, the mechanism by
which arsenite causes cancer is not well understood. In this study, we
found that exposure of Cl 41 cells, a well characterized mouse
epidermal cell model for tumor promotion, to a low concentration of
arsenite (<25 µM) induces cell transformation.
Interestingly, arsenite induces Erk phosphorylation and increased Erk
activity at doses ranging from 0.8 to 200 µM, while
higher doses (more than 50 µM) are required for
activation of JNK. Arsenite-induced Erk activation was markedly
inhibited by introduction of dominant negative Erk2 into cells, while
expression of dominant negative Erk2 did not show inhibition of JNK and
MEK1/2. Furthermore, arsenite-induced cell
transformation was blocked in cells expressing the dominant negative
Erk2. In contrast, overexpression of dominant negative JNK1 was shown
to increase cell transformation even though it inhibits
arsenite-induced JNK activation. Our results not only show that
arsenite induces Erk activation, but also for the first time
demonstrates that activation of Erk, but not JNK, by arsenite is
required for its effects on cell transformation.
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