Regulation of Retinoic Acid-induced Inhibition of AP-1 Activity by Orphan Receptor Chicken Ovalbumin Upstream Promoter-Transcription Factor

Lin, Feng; Kolluri, Siva Kumar; Chen, Guoquan; Zhang, Xiaokun

doi:10.1074/jbc.m201885200

Cited by 20 publications

(19 citation statements)

References 46 publications

(78 reference statements)

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“…These include binding sites for chicken ovalbumin upstream promoter-transcription factor and hepatocyte nuclear factor-1. Both of these factors are expressed in the kidney (Baumhueter et al 1990, Suzuki et al 2000 and both have been previously shown to physically interact with members of the AP-1 transcription factor family (Leu et al 2001, Lin et al 2002.…”

Section: Discussionmentioning

confidence: 99%

Insulin-mediated activation of activator protein-1 through the mitogen-activated protein kinase pathway stimulates collagenase-1 gene transcription in the MES 13 mesangial cell line

Ayala

Boustead²,

Chapman³

et al. 2004

Journal of Molecular Endocrinology

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The initial stages of diabetic nephropathy are characterized, in part, by expansion of the mesangial matrix and thickening of the glomerular basement membrane which are caused by increased extracellular matrix (ECM) protein synthesis and reduced degradation, a consequence of decreased matrix metalloproteinase (MMP) activity. These changes have been largely attributed to the effects of hyperglycemia such that the potential contribution of impaired insulin action to alterations in the ECM have not been studied in detail. We have shown here that insulin stimulates collagenase-1 fusion gene transcription in the MES 13 mesangial-derived cell line. Multiple collagenase-1 promoter elements are required for the full stimulatory effect of insulin but the action of insulin appears to be mediated through an activator protein-1 (AP-1) motif. Thus, mutation of this AP-1 motif abolishes insulin-stimulated collagenase fusion gene transcription and, in isolation, this AP-1 motif can mediate a stimulatory effect of insulin on the expression of a heterologous fusion gene. This suggested that the other collagenase-1 promoter elements that are required for the full stimulatory effect of insulin probably bind accessory factors that enhance the effect of insulin mediated through the AP-1 motif. In MES 13 cells, the AP-1 motif is bound by Fra-1, Fra-2, Jun B and Jun D. Stimulation of collagenase-1 fusion gene transcription by insulin requires activation of the mitogen-activated protein kinase (MEK) pathway since inhibition of MEK-1 and -2 blocks this effect. The potential significance of these observations with respect to a role for insulin in the pathophysiology of diabetic glomerulosclerosis is discussed.

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Section: Discussionmentioning

confidence: 99%

Insulin-mediated activation of activator protein-1 through the mitogen-activated protein kinase pathway stimulates collagenase-1 gene transcription in the MES 13 mesangial cell line

Ayala

Boustead²,

Chapman³

et al. 2004

Journal of Molecular Endocrinology

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“…The target sequence of the COUP-TFII shRNA construct was 5Ј-AGCT-CTTGCTTCGTCTCCC-3Ј. The COUP-TFII mutant constructs for this study were COUP-TFII⌬DBD (DNA binding domain deletion mutant), COUP-TFII⌬N75 (N-terminal deletion mutant), and COUP-TFII⌬179 (C-terminal deletion mutant), which were described previously (16,17).…”

Section: Methodsmentioning

confidence: 99%

Orphan Nuclear Receptor Chicken Ovalbumin Upstream Promoter-Transcription Factor II (COUP-TFII) Protein Negatively Regulates Bone Morphogenetic Protein 2-induced Osteoblast Differentiation through Suppressing Runt-related Gene 2 (Runx2) Activity

Lee

Jang

Kim

et al. 2012

Journal of Biological Chemistry

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Background: COUP-TFII, an orphan nuclear receptor, regulates the differentiation process in various cell types during development. Results: COUP-TFII inhibits Runx2-dependent osteocalcin transcription through physical interaction with Runx2 and matrix mineralization. Conclusion: COUP-TFII is a negative regulator of osteoblast differentiation. Significance: COUP-TFII has therapeutic potential for controlling bone-related disease.

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“…COUP-TF interacts with other nuclear receptors, including ER, the retinoid X receptor, peroxisome proliferator-activated receptors, and the vitamin D receptor (18)(19)(20)(21), via direct interaction with receptor ligand-binding domain (22). In general, COUP-TF inhibits the transcriptional activity of other nuclear receptors by competing for their DNA binding sites or by heterodimerization with the class II nuclear receptor heterodimer partner retinoid X receptor, thereby preventing gene expression (22).…”

Section: Introductionmentioning

confidence: 99%

Decreased Chicken Ovalbumin Upstream Promoter Transcription Factor II Expression in Tamoxifen-Resistant Breast Cancer Cells

Riggs

Wickramasinghe²,

Cochrum³

et al. 2006

Cancer Research

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Tamoxifen (TAM) is successfully used for the treatment and prevention of breast cancer. However, many patients that are initially TAM responsive develop tumors that are antiestrogen/TAM resistant (TAM-R). The mechanism behind TAM resistance in estrogen receptor A (ERA)-positive tumors is not understood. The orphan nuclear receptor chicken ovalbumin upstream promoter transcription factor (COUP-TF)-I interacts directly with 4-hydroxytamoxifen (4-OHT)-and estradiol (E 2 )-occupied ERA, corepressors NCoR and SMRT, and inhibit E 2 -induced gene transcription in breast cancer cells. Here we tested the hypothesis that reduced COUP-TFI and COUP-TFII correlate with TAM resistance. We report for the first time that COUP-TFII, but not COUP-TFI, is reduced in three antiestrogen/TAM-R cell lines derived from TAMsensitive (TAM-S) MCF-7 human breast cancer cells and in MDA-MB-231 cells compared with MCF-7. ERA and ERB protein expression was not different between TAM-S and TAM-R cells, but progesterone receptor (PR) was decreased in TAM-R cells. Further, E 2 increased COUP-TFII transcription in MCF-7, but not TAM-R, cells. Importantly, reexpression of COUP-TFII in TAM-S cells to levels comparable to those in MCF-7 was shown to increase 4-OHT-mediated growth inhibition and increased apoptosis. Conversely, knockdown of COUP-TFII in TAM-S MCF-7 cells blocked growth inhibitory activity and increased 4-OHT agonist activity. 4-OHT increased COUP-TFII-ERA interaction f2-fold in MCF-7 cells. COUP-TFII expression in TAM-R cells also inhibited 4-OHT-induced endogenous PR and pS2 mRNA expression. These data indicate that reduced COUP-TFII expression correlates with acquired TAM resistance in human breast cancer cell lines and that COUP-TFII plays a role in regulating the growth inhibitory activity of TAM in breast cancer cells.

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Regulation of Retinoic Acid-induced Inhibition of AP-1 Activity by Orphan Receptor Chicken Ovalbumin Upstream Promoter-Transcription Factor

Cited by 20 publications

References 46 publications

Insulin-mediated activation of activator protein-1 through the mitogen-activated protein kinase pathway stimulates collagenase-1 gene transcription in the MES 13 mesangial cell line

Insulin-mediated activation of activator protein-1 through the mitogen-activated protein kinase pathway stimulates collagenase-1 gene transcription in the MES 13 mesangial cell line

Orphan Nuclear Receptor Chicken Ovalbumin Upstream Promoter-Transcription Factor II (COUP-TFII) Protein Negatively Regulates Bone Morphogenetic Protein 2-induced Osteoblast Differentiation through Suppressing Runt-related Gene 2 (Runx2) Activity

Decreased Chicken Ovalbumin Upstream Promoter Transcription Factor II Expression in Tamoxifen-Resistant Breast Cancer Cells

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