p42/p44 MAP Kinase Module Plays a Key Role in the Transcriptional Regulation of the Vascular Endothelial Growth Factor Gene in Fibroblasts

Milanini, Julie; Viñals, Francesc; Pouysségur, Jacques; Pagès, Gilles

doi:10.1074/jbc.273.29.18165

Cited by 285 publications

(258 citation statements)

References 56 publications

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“…We previously showed that VEGF is up-regulated in serum-starved HT29 cells through the activation of Erk-1 and Erk-2 (Jung et al, 1999). Milanini et al (1998) also found that maximal transcriptional activation of VEGF in fibroblasts was Erk-dependent. The EGCG-mediated inhibition of Erk-1 and -2 activation may be an early cellular event that is partly responsible for the anticancer effect of EGCG.…”

Section: Discussionmentioning

confidence: 85%

“…Blockade of the Mek-Erk pathway suppresses growth of colon tumours in vivo (SeboltLeopold et al, 1999). Recently, Erk-1 and Erk-2 has been reported to be an important signalling cascade that leads to overexpression of VEGF mRNA (Jung et al, 1999;Milanini et al, 1998). We previously showed that VEGF is up-regulated in serum-starved HT29 cells through the activation of Erk-1 and Erk-2 (Jung et al, 1999).…”

Section: Discussionmentioning

confidence: 95%

“…Activation of Erk-1 and Erk-2 have been shown to be important mediators for up-regulation of VEGF mRNA. Milanini et al (1998) demonstrated that activation of Erk-1 and Erk-2 play a key role in the regulation of the VEGF expression via alteration of AP-2 and Sp1 transcription factors in fibroblasts. Our previous studies on VEGF induction in serum-starved cells revealed a causal role for the activation of Erk -but not of P38, stress-activated protein kinase (SAPK) or Akt (Jung et al, 1999).…”

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confidence: 99%

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EGCG, a major component of green tea, inhibits tumour growth by inhibiting VEGF induction in human colon carcinoma cells

et al. 2001

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Catechins are key components of teas that have antiproliferative properties. We investigated the effects of green tea catechins on intracellular signalling and VEGF induction in vitro in serum-deprived HT29 human colon cancer cells and in vivo on the growth of HT29 cells in nude mice. In the in vitro studies, (-)-epigallocatechin gallate (EGCG), the most abundant catechin in green tea extract, inhibited Erk-1 and Erk-2 activation in a dose-dependent manner. However, other tea catechins such as (-)-epigallocatechin (EGC), (-)-epicatechin gallate (ECG), and (-)-epicatechin (EC) did not affect Erk-1 or 2 activation at a concentration of 30 μM. EGCG also inhibited the increase of VEGF expression and promoter activity induced by serum starvation. In the in vivo studies, athymic BALB/c nude mice were inoculated subcutaneously with HT29 cells and treated with daily intraperitoneal injections of EC (negative control) or EGCG at 1.5 mg day −1 mouse −1 starting 2 days after tumour cell inoculation. Treatment with EGCG inhibited tumour growth (58%), microvessel density (30%), and tumour cell proliferation (27%) and increased tumour cell apoptosis (1.9-fold) and endothelial cell apoptosis (3-fold) relative to the control condition ( P < 0.05 for all comparisons). EGCG may exert at least part of its anticancer effect by inhibiting angiogenesis through blocking the induction of VEGF. © 2001 Cancer Research Campaign http://www.bjcancer.com

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Section: Discussionmentioning

confidence: 85%

Section: Discussionmentioning

confidence: 95%

mentioning

confidence: 99%

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EGCG, a major component of green tea, inhibits tumour growth by inhibiting VEGF induction in human colon carcinoma cells

et al. 2001

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“…MKK activity regulates VEGF expression at the transcriptional and post-transcriptional levels (Pages et al, 2000). Expression of constitutively active MEK1 in fibroblasts elevates expression of VEGF mRNA through binding of the transcription factors Sp1 and AP-2 to its promoter region (Milanini et al, 1998). Also, VEGF mRNA half-life is increased in cells that overexpress p38 MAPK and JNK (Pages et al, 2000).…”

Section: Mkk Signaling and Tumor Vascularizationmentioning

confidence: 99%

MKK signaling and vascularization

et al. 2007

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In 1998, George Vande Woude's lab discovered that anthrax lethal factor (LF), the principal virulence component of anthrax toxin, was a zinc-metalloprotease that cleaved and inactivated mitogen-activated protein kinase kinases (MKK). It was perhaps not surprising, given the known roles of MKK1 and 2 in cell proliferation, that LF was subsequently found to dramatically inhibit tumor growth in vivo. What was not anticipated, however, was that the tumors treated with LF would have a substantially reduced vascular content. This intriguing result was one of the first indications that MKK signaling plays an important role in promoting tumor vascularization in vivo. In the following short review, we will compare in vitro and in vivo evidence that supports the hypothesis that MKK signaling pathways are essential for vascularization.

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“…The VEGF-luciferase reporter was a kind gift of Darren Richard. It contains the upstream sequence from the human VEGF gene (44). STAT cDNA vectors expressing wild-type proteins from Svsport1 were provided by Juergen A. Ripperger.…”

Section: Methodsmentioning

confidence: 99%

Convergence of Protein Kinase C and JAK-STAT Signaling on Transcription Factor GATA-4

Wang

Paradis

Aries

et al. 2005

Molecular and Cellular Biology

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Angiotensin II (AII), a potent vasoactive hormone, acts on numerous organs via G-protein-coupled receptors and elicits cell-specific responses. At the level of the heart, AII stimulation alters gene transcription and leads to cardiomyocyte hypertrophy. Numerous intracellular signaling pathways are activated in this process; however, which of these directly link receptor activation to transcriptional regulation remains undefined. We used the atrial natriuretic factor (ANF) gene (NPPA) as a marker to elucidate the signaling cascades involved in AII transcriptional responses. We show that ANF transcription is activated directly by the AII type 1 receptor and precedes the development of myocyte hypertrophy. This response maps to STAT and GATA binding sites, and the two elements transcriptionally cooperate to mediate signaling through the JAK-STAT and protein kinase C (PKC)-GATA-4 pathways. PKC phosphorylation enhances GATA-4 DNA binding activity, and STAT-1 functionally and physically interacts with GATA-4 to synergistically activate AII and other growth factor-inducible promoters. Moreover, GATA factors are able to recruit STAT proteins to target promoters via GATA binding sites, which are sufficient to support synergy. Thus, STAT proteins can act as growth factor-inducible coactivators of tissue-specific transcription factors. Interactions between STAT and GATA proteins may provide a general paradigm for understanding cell specificity of cytokine and growth factor signaling.

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p42/p44 MAP Kinase Module Plays a Key Role in the Transcriptional Regulation of the Vascular Endothelial Growth Factor Gene in Fibroblasts

Cited by 285 publications

References 56 publications

EGCG, a major component of green tea, inhibits tumour growth by inhibiting VEGF induction in human colon carcinoma cells

EGCG, a major component of green tea, inhibits tumour growth by inhibiting VEGF induction in human colon carcinoma cells

MKK signaling and vascularization

Convergence of Protein Kinase C and JAK-STAT Signaling on Transcription Factor GATA-4

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