Inhibition of Tissue Factor Gene Activation in Cultured Endothelial Cells by Curcumin

Pendurthi, Usha R.; Williams, J. Todd; Rao, L. Vijaya Mohan

doi:10.1161/01.atv.17.12.3406

Cited by 112 publications

(28 citation statements)

References 39 publications

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“…The current report demonstrated that curcumin significantly suppressed gene expression of Egr-1 at both transcription and translation levels (Figure 7), which is consistent with previous other reports ( Pendurthi et al, 1997;Han et al, 1999;Pendurthi and Rao, 2000). Others and we have previously demonstrated that curcumin effectively inhibits the ERK activity in a Curcumin suppresses expression of egfr A Chen et al variety of cells, including colon cancer cells (Chen and Tan, 1998;Chen et al, 1999;Jobin et al, 1999).…”

Section: Discussionsupporting

confidence: 92%

Curcumin inhibits human colon cancer cell growth by suppressing gene expression of epidermal growth factor receptor through reducing the activity of the transcription factor Egr-1

2005

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High expression of epidermal growth factor receptor (EGFR) is found in a variety of solid tumors, including colorectal cancer. EGFR has been identified as a rational target for anticancer therapy. Curcumin, the yellow pigment of turmeric in curry, has received attention as a promising dietary supplement for cancer prevention and treatment. We recently reported that curcumin inhibited the growth of human colon cancer-derived Moser cells by suppressing gene expression of cyclinD1 and EGFR. The aim of the present study was to explore the molecular mechanisms underlying curcumin inhibition of gene expression of EGFR in colon cancer cells. The generality of the inhibitory effect of curcumin on gene expression of EGFR was verified in other human colon cancer-derived cell lines, including Caco-2 and HT-29 cells. Promoter deletion assays and sitedirected mutageneses identified a binding site for the transcription factor early growth response-1 (Egr-1) in egfr promoter as a putative curcumin response element in regulating the promoter activity of the gene in Moser cells. Electrophoretic mobility shift assays demonstrated that curcumin significantly reduced the DNA-binding activity of the transcription factor Egr-1 to the curcumin response element. In addition, curcumin reduced the trans-activation activity of Egr-1 by suppressing egr-1 gene expression, which required interruption of the ERK signal pathway and reduction of the level of phosphorylation of Elk-1 and its activity. Taken together, our results demonstrated that curcumin inhibited human colon cancer cell growth by suppressing gene expression of EGFR through reducing the trans-activation activity of Egr-1. These results provided novel insights into the mechanisms of curcumin inhibition of colon cancer cell growth and potential therapeutic strategies for treatment of colon cancer.

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Section: Discussionsupporting

confidence: 92%

Curcumin inhibits human colon cancer cell growth by suppressing gene expression of epidermal growth factor receptor through reducing the activity of the transcription factor Egr-1

2005

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“…Competitive binding of angiostatin and plasminogen to annexin II may cause the reduced production of plasmin. Interestingly, a link between plasmin and the activation of ERK was provided by Pendurthi et al (38), who reported that plasmin is able to induce the activation of ERK1/2 through the protease-activated receptor 1. Similarly, apo(a) has also been reported to interfere with plasmin generation on endothelial cell surfaces by binding to annexin II (39).…”

Section: Discussionmentioning

confidence: 99%

Inhibition of Angiogenesis and Angiogenesis-dependent Tumor Growth by the Cryptic Kringle Fragments of Human Apolipoprotein(a)

Kim

Chang²,

Yu³

et al. 2003

Journal of Biological Chemistry

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Apolipoprotein(a) (apo(a)) contains tandemly repeated kringle domains that are closely related to plasminogen kringle 4, followed by a single kringle 5-like domain and an inactive protease-like domain. Recently, the anti-angiogenic activities of apo(a) have been demonstrated both in vitro and in vivo. However, its effects on tumor angiogenesis and the underlying mechanisms involved have not been fully elucidated. To evaluate the anti-angiogenic and anti-tumor activities of the apo(a) kringle domains and to elucidate their mechanism of action, we expressed the last three kringle domains of apo(a), KIV-9, KIV-10, and KV, in Escherichia coli. The resultant recombinant protein, termed rhLK68, exhibited a dose-dependent inhibition of basic fibroblast growth factor-stimulated human umbilical vein endothelial cell proliferation and migration in vitro and inhibited the neovascularization in chick chorioallantoic membranes in vivo. The ability of rhLK68 to abrogate the activation of extracellular signal-regulated kinases appears to be responsible for rhLK68-mediated anti-angiogenesis. Furthermore, systemic administration of rhLK68 suppressed human lung (A549) and colon (HCT-15) tumor growth in nude mice. Immunohistochemical examination and in situ hybridization analysis of the tumors showed a significant decrease in the number of blood vessels and the reduced expression of vascular endothelial growth factor, basic fibroblast growth factor, and angiogenin, indicating that suppression of angiogenesis may have played a significant role in the inhibition of tumor growth. Collectively, these results suggest that a truncated apo(a), rhLK68, is a potent antiangiogenic and anti-tumor molecule.

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“…Thus, curcuminoids have been shown to inhibit activation of these transcription factors in response to phorbol myristate acetate (PMA), tumor necrosis factor-␣, and hydrogen peroxide (25,26). In vascular endothelial cells, curcuminoids reduce the activation of tissue factor gene expression induced by tumor necrosis factor-␣, lipopolysaccharide, PMA, and thrombin resulting from the coordinate inhibition of AP-1 DNA binding activity and nuclear translocation of NF-B (27,28).…”

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confidence: 99%

Curcuminoids Inhibit the Angiogenic Response Stimulated by Fibroblast Growth Factor-2, Including Expression of Matrix Metalloproteinase Gelatinase B

Mohan¹,

Sivak²,

Ashton³

et al. 2000

Journal of Biological Chemistry

231

126

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We have studied mechanisms controlling activation of the gelatinase B gene (matrix metalloproteinase-9) by fibroblast growth factor-2 (FGF-2) during angiogenesis, and the effects of the natural product curcuminoids on this process. Using a transgenic mouse (line 3445) harboring a gelatinase B promoter/lacZ fusion gene, we demonstrate FGF-2 stimulation of reporter gene expression in endothelial cells of invading neocapillaries in the corneal micropocket assay. Using cultured corneal cells, we show that FGF-2 stimulates DNA binding activity of transcription factor AP-1 but not NF-B and that AP-1 stimulation is inhibited by curcuminoids. We further show that induction of gelatinase B transcriptional promoter activity in response to FGF-2 is dependent on AP-1 but not NF-B response elements and that promoter activity is also inhibited by curcuminoids. In rabbit corneas, the angiogenic response induced by implantation of an FGF-2 pellet is inhibited by the coimplantation of a curcuminoid pellet, and this correlates with inhibition of endogenous gelatinase B expression induced by FGF-2. Angiostatic efficacy in the cornea is also observed when curcuminoids are provided to mice in the diet. Our findings provide evidence that curcuminoids target the FGF-2 angiogenic signaling pathway and inhibit expression of gelatinase B in the angiogenic process.

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Inhibition of Tissue Factor Gene Activation in Cultured Endothelial Cells by Curcumin

Cited by 112 publications

References 39 publications

Curcumin inhibits human colon cancer cell growth by suppressing gene expression of epidermal growth factor receptor through reducing the activity of the transcription factor Egr-1

Curcumin inhibits human colon cancer cell growth by suppressing gene expression of epidermal growth factor receptor through reducing the activity of the transcription factor Egr-1

Inhibition of Angiogenesis and Angiogenesis-dependent Tumor Growth by the Cryptic Kringle Fragments of Human Apolipoprotein(a)

Curcuminoids Inhibit the Angiogenic Response Stimulated by Fibroblast Growth Factor-2, Including Expression of Matrix Metalloproteinase Gelatinase B

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