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Abstract
Metastatic mouse mammary tumor cell line 4526 was used to determine whether linoleate
(LN)-derived cyclooxygenase metabolites were involved in the mechanism of LN-enhanced
4526 tumor growth. Unstimulated line 4526 cells converted LN to both PGE1 and PGE2 in serum free medium (SFM). However, neither prostaglandin (PG) influenced growth,
while db-cGMP, but not db-cAMP, stimulated growth to the same extent as LN. Cyclooxygenase
inhibitors stimulated growth while suppressing PG synthesis. Lipoxygenase inhibitors
decreased growth in a dose dependent manner. Supplemental LN had no effect on cyclooxygenase
inhibition while the IC50s for lipoxygenase inhibition were increased several fold. These results indicate
that lipoxygenase products rather than cyclooxygenase metabolites play a major role
in LN-stimulated growth of line 4526 cells.
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receptor and tumor cell adhesion by lipoxygenase products of arachidonic acid and linoleic acid.Article info
Publication history
Accepted:
July 3,
1991
Received:
May 22,
1991
Identification
Copyright
© 1991 Published by Elsevier Inc.
