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Ligand, 15-Deoxy-
12,14- prostaglandin J21
Departments of Urology [R. B., S. H. M., D. J. T., C. Y. F. Y.] and Biochemistry [D. J. T., C. Y. F. Y.] and Molecular Biology, Mayo Clinic/Foundation, Rochester, Minnesota 55905
Abstract
15-Deoxy-
12,14-prostaglandin J2
(15d-PGJ2) is a highly specific activator of the peroxisome
proliferator-activated receptor 
(PPAR-). We investigated the
effect of 15d-PGJ2 on three human prostate cancer cell
lines, LNCaP, DU145, and PC-3. Western blotting demonstrated that
PPAR-1 is expressed predominantly in untreated prostate cancer
cells. Treatment with 15d-PGJ2 caused an increase in the
expression of PPAR-2, whereas PPAR-1 remained at basal levels.
PPARs 
and ß were not detected in these cells. Lack of lipid
accumulation, increase in CCAAT/enhancer binding proteins (C/EBPs), or
expression of aP2 mRNA indicated that adipocytic differentiation is not
induced in these cells by 15d-PGJ2. 15d-PGJ2
and other PPAR- activators induced cell death in all three cell
lines at concentrations as low as 2.5 µM (similar to the
Kd of PPAR- for this ligand), coinciding
with an accumulation of cells in the S-phase of the cell cycle.
Activators for PPAR- and ß did not induce cell death. Staining
with trypan blue and propidium iodide suggested that, although the
plasma membrane appears intact by electron microscopy, disturbances are
evident as early as 2 h after treatment. Mitochondrial
transmembrane potentials are significantly reduced by
15d-PGJ2 treatment. In addition, treatment with
15d-PGJ2 resulted in cytoplasmic changes, which are
indicative of type 2 (autophagic), nonapoptotic programmed cell death.
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| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
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| Cancer Epidemiology Biomarkers & Prevention | Molecular Cancer Therapeutics |
| Molecular Cancer Research | Cell Growth & Differentiation |
