The PPAR Gamma Agonist Troglitazone Regulates Erk 1/2 Phosphorylation via a PPARγ-Independent, MEK-Dependent Pathway in Human Prostate Cancer Cells

Thiazolidinediones (TZDs) dramatically reduce the growth of human prostate cancer cellsin vitroandin vivo. To determine whether the antitumor effects of TZDs were due in part to changes in the MEK/Erk signaling pathway, we examined the regulation of Erk phosphorylation by the TZD troglitazone within the PC-3 and C4-2 human prostate cancer cell lines. Western blot analysis revealed troglitazone-induced phosphorylation of Erk in both PC-3 and C4-2 cells. Troglitazone-induced increases in Erk phosphorylation were suppressed by the MEK inhibitor U0126 but not by the PPARγantagonist GW9662. Pretreatment with U0126 did not alter the ability of troglitazone to regulate expression of two proteins that control cell cycle, p21, and c-Myc. Troglitazone was also still effective at reducing PC-3 proliferation in the presence of U0126. Therefore, our data suggest that troglitazone-induced Erk phosphorylation does not significantly contribute to the antiproliferative effect of troglitazone.

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Differential effects of transforming growth factor β on human prostate cancer cells in vitro

Molecular and Cellular Endocrinology ◽

10.1016/0303-7207(89)90115-9 ◽

1989 ◽

Vol 62 (1) ◽

pp. 79-87 ◽

Cited By ~ 111

Author(s):

George Wilding ◽

Gerhard Zugmeier ◽

Cornelius Knabbe ◽

Katherine Flanders ◽

Edward Gelmann

Keyword(s):

Prostate Cancer ◽

Growth Factor ◽

Cancer Cells ◽

Transforming Growth Factor ◽

Transforming Growth Factor Β ◽

Human Prostate ◽

Human Prostate Cancer ◽

Prostate Cancer Cells ◽

Differential Effects

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ANTITUMOR EFFECTS OF CHRYSANTHEMIN IN PC-3 HUMAN PROSTATE CANCER CELLS ARE MEDIATED VIA APOPTOSIS INDUCTION, CASPASE SIGNALLING PATHWAY AND LOSS OF MITOCHONDRIAL MEMBRANE POTENTIAL

African Journal of Traditional Complementary and Alternative Medicines ◽

10.21010/ajtcam.v14i4.7 ◽

2017 ◽

Vol 14 (4) ◽

pp. 54-61 ◽

Cited By ~ 4

Author(s):

De-Kang Sun ◽

Lin Wang ◽

Pen Zhang

Keyword(s):

Prostate Cancer ◽

Membrane Potential ◽

Cancer Cells ◽

Mitochondrial Membrane Potential ◽

Mitochondrial Membrane ◽

Human Prostate ◽

Human Prostate Cancer ◽

Apoptosis Induction ◽

Prostate Cancer Cells ◽

Antitumor Effects

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Blueberry flavonoids inhibit matrix metalloproteinase activity in DU145 human prostate cancer cells

Biochemistry and Cell Biology ◽

10.1139/o05-063 ◽

2005 ◽

Vol 83 (5) ◽

pp. 637-643 ◽

Cited By ~ 47

Author(s):

Michael D Matchett ◽

Shawna L MacKinnon ◽

Marva I Sweeney ◽

Katherine T Gottschall-Pass ◽

Robert A.R Hurta

Keyword(s):

Prostate Cancer ◽

Cancer Cells ◽

Apoptotic Cell ◽

Human Prostate ◽

Response To Treatment ◽

Human Prostate Cancer ◽

Prostate Cancer Cells ◽

The Matrix ◽

Ecm Degradation

Regulation of the matrix metalloproteinases (MMPs), the major mediators of extracellular matrix (ECM) degradation, is crucial to regulate ECM proteolysis, which is important in metastasis. This study examined the effects of 3 flavonoid-enriched fractions (a crude fraction, an anthocyanin-enriched fraction, and a proanthocyanidin-enriched fraction), which were prepared from lowbush blueberries (Vaccinium angustifolium), on MMP activity in DU145 human prostate cancer cells in vitro. Using gelatin gel electrophoresis, MMP activity was evaluated from cells after 24-hr exposure to blueberry fractions. All fractions elicited an ability to decrease the activity of MMP-2 and MMP-9. Of the fractions tested, the proanthocyanidin-enriched fraction was found to be the most effective at inhibiting MMP activity in these cells. No induction of either necrotic or apoptotic cell death was noted in these cells in response to treatment with the blueberry fractions. These findings indicate that flavonoids from blueberry possess the ability to effectively decrease MMP activity, which may decrease overall ECM degradation. This ability may be important in controlling tumor metastasis formation.Key words: blueberry flavonoids, MMP activity, prostate cancer cells.

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