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(Received for publication, October 17, 1996, and in revised form, January 7, 1997)
From The Hormel Institute, University of Minnesota,
Austin, Minnesota 55912
Aspirin, along with its analgesic-antipyretic
uses, is now also being considered for prevention of cardiovascular
disease, cancer, and treatment of human immunodeficiency virus
infection. Although many of aspirin's pharmacological actions are
related to its ability to inhibit prostaglandin biosynthesis, some of its beneficial therapeutic effects are not completely understood. Transcription factor activator protein 1 (AP-1) is critical for the
induction of neoplastic transformation and induction of multiple genes
involved in inflammation and infection. We have used the JB6 mouse
epidermal cell lines, a system that has been used extensively as an
in vitro model for the study of tumor promotion and
anti-tumor promotion, to study the anti-carcinogenesis effect of
aspirin at the molecular level. Aspirin and aspirin-like salicylates
inhibited the activation of AP-1 in the same dose range as seen for the inhibition of tumor promoter-induced transformation. The inhibition of
AP-1 and tumor promoter-induced transformation in JB6 cells occurs
through a prostaglandin independent- and an Erk1- or Erk2-independent pathway. The mechanism of AP-1 and transformation inhibition in this
cell culture model may involve the elevation of H+
concentration. The inhibition effects on the activation of AP-1 activity by aspirin and aspirin-like salicylates may further explain the anti-carcinogenesis mechanism of action of these drugs.
Volume 272, Number 15,
Issue of April 11, 1997
pp. 9962-9970
©1997 by The American Society for Biochemistry and Molecular Biology, Inc.
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