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.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 177-184 |
| Number of pages | 8 |
| Journal | Prostaglandins, Leukotrienes and Essential Fatty Acids |
| Volume | 44 |
| Issue number | 3 |
| DOIs | |
| State | Published - 1991 |
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ASJC Scopus subject areas
- Clinical Biochemistry
- Endocrinology, Diabetes and Metabolism
Cite this
Eicosanoids and linoleate-enhanced growth of mouse mammary tumor cells. / Buckman, D. K.; Hubbard, Neil; Erickson, Kent L.
In: Prostaglandins, Leukotrienes and Essential Fatty Acids, Vol. 44, No. 3, 1991, p. 177-184.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Eicosanoids and linoleate-enhanced growth of mouse mammary tumor cells
AU - Buckman, D. K.
AU - Hubbard, Neil
AU - Erickson, Kent L
PY - 1991
Y1 - 1991
N2 - 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.
AB - 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.
UR - http://www.scopus.com/inward/record.url?scp=0026077142&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0026077142&partnerID=8YFLogxK
U2 - 10.1016/0952-3278(91)90053-8
DO - 10.1016/0952-3278(91)90053-8
M3 - Article
C2 - 1667043
AN - SCOPUS:0026077142
VL - 44
SP - 177
EP - 184
JO - Prostaglandins Leukotrienes and Essential Fatty Acids
JF - Prostaglandins Leukotrienes and Essential Fatty Acids
SN - 0952-3278
IS - 3
ER -