New and known symmetrical curcumin derivatives inhibit the formation of Fos-Jun-DNA complex

Hahm, Eun‐Ryeong; Cheon, Gyo; Lee, Juhyung; Kim, Bonjoong; Park, Chihoon; Yang, Chung-May

doi:10.1016/s0304-3835(02)00170-2

Cited by 60 publications

(48 citation statements)

References 13 publications

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“…However, pretreatment of cells with curcumin abolished the mimosine-induced AP-1 binding activity. This observation is consistent with the previous findings (33,34). We next determined the expression level of Drg-1 following these treatments.…”

Section: Comparison Of the Effects Of Mimosine On Drg-1 Expression Wisupporting

confidence: 92%

“…To further confirm that the transcription factor AP-1 mediates the mimosine-induced transcription of Drg-1, we performed another experiment to determine whether the mimosine-induced Drg-1 expression can be blocked by inhibiting AP-1 activity using curcumin, a yellow pigment of turmeric that inhibits formation of AP-1⅐DNA complex (33,34). As shown in Fig.…”

Section: Comparison Of the Effects Of Mimosine On Drg-1 Expression Wimentioning

confidence: 99%

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Modulation of Differentiation-related Gene 1 Expression by Cell Cycle Blocker Mimosine, Revealed by Proteomic Analysis

Dong

Arnold

Yang

et al. 2005

Molecular & Cellular Proteomics

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L-Mimosine, a plant amino acid, can reversibly block mammalian cells at late G 1 phase and has been found to affect translation of mRNAs of the cyclin-dependent kinase inhibitor p27, eIF3a (eIF3 p170), and ribonucleotide reductase M2. The effect of mimosine on the expression of these genes may be essential for the G 1 phase arrest. To determine additional genes that may be early respondents to the mimosine treatment, we performed two-dimensional gel electrophoretic analysis of [35 S]methionine-labeled cell lysates followed by identification of the altered protein spots by LC-tandem mass spectrometry. In this study, the synthesis of two protein spots (MIP42 and MIP17) was found to be enhanced by mimosine, whereas the formation of another protein spot (MSP17) was severely blocked following mimosine treatment. These protein spots, MIP42, MIP17, and MSP17, were identified to be differentiation-related gene 1 (Drg-1; also called RTP, cap43, rit42, Ndrg-1, and PROXY-1), deoxyhypusine-containing eIF5A intermediate, and mature hypusine-containing eIF5A, respectively. The effect of mimosine on eIF5A maturation was due to inhibition of deoxyhypusine hydroxylase, the enzyme catalyzing the final step of hypusine biosynthesis in eIF5A. The mimosine-induced expression of Drg-1 was mainly attributable to increased transcription likely by the c-Jun/AP-1 transcription factor. Because induction of Drg-1 is an early event after mimosine treatment and is observed before a notable reduction in the steady-state level of mature eIF5A, eIF5A does not appear to be involved in the modulation of Drg-1 expression. Molecular & Cellular Proteomics 4:993-1001, 2005.

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Section: Comparison Of the Effects Of Mimosine On Drg-1 Expression Wisupporting

confidence: 92%

Section: Comparison Of the Effects Of Mimosine On Drg-1 Expression Wimentioning

confidence: 99%

Modulation of Differentiation-related Gene 1 Expression by Cell Cycle Blocker Mimosine, Revealed by Proteomic Analysis

Dong

Arnold

Yang

et al. 2005

Molecular & Cellular Proteomics

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“…Neurotensin increases AP-1 DNA-binding activity, which involves c-Fos, JunB, and Fra-1 proteins. Hahm et al (34) reported that curcumin can inhibit the formation of the Fos-Jun DNA complex, thus suppressing AP-1-regulated gene expression. As shown in Fig.…”

Section: Resultsmentioning

confidence: 99%

Curcumin Inhibits Neurotensin-Mediated Interleukin-8 Production and Migration of HCT116 Human Colon Cancer Cells

Wang¹,

Wang²,

Ives³

et al. 2006

Clinical Cancer Research

101

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Purpose: Neurotensin, a gut tridecapeptide, acts as a potent cellular mitogen for various colorectal and pancreatic cancers that possess high-affinity neurotensin receptors. Cytokine/ chemokine proteins are increasingly recognized as important local factors that play a role in the metastasis and invasion of multiple cancers. The purpose of this study was to (a) determine the effect of neurotensin on cytokine/chemokine gene expression and cell migration in human cancer cells and (b) assess the effect of curcumin, a natural dietary product, on neurotensinmediated processes. Experimental Design: The human colorectal cancer, HCT116, was treated with neurotensin, with or without curcumin, and interleukin (IL)-8 expression and protein secretion was measured. Signaling pathways, which contribute to the effects of neurotensin, were assessed. Finally, the effect of curcumin on neurotensin-mediated HCT116 cell migration was analyzed. Results: We show that neurotensin, acting through the native high-affinity neurotensin receptor, induced IL-8 expression in human colorectal cancer cells in a time-and dose-dependent fashion. This stimulation involves Ca 2+ -dependent protein kinase C, extracellular signal-regulated kinased ependent activator protein-1, and extracellular signal-regulated kinase^independent nuclear factor-nB pathways. Curcumin inhibited neurotensin-mediated activator protein-1 and nuclear factor-nB activation and Ca 2+ mobilization. Moreover, curcumin blocked neurotensin-stimulated IL-8 gene induction and protein secretion and, at a low concentration (i.e., 10 Amol/L), blocked neurotensin-stimulated colon cancer cell migration. Conclusions: Neurotensin-mediated induction of tumor cell IL-8 expression and secretion may contribute to the procarcinogenic effects of neurotensin on gastrointestinal cancers. Furthermore, a potential mechanism for the chemopreventive and chemotherapeutic effects of curcumin on colon cancers may be through the inhibition of gastrointestinal hormone (e.g., neurotensin)î nduced chemokine expression and cell migration.

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“…Then we further tested whether AP1 and NF-κB were also involved in TNF-α-induced human amylin expression. Pretreatment of −222/450 construct-transfected MIN6 cells with curcumin (AP1 inhibitor) [33] or sulfasalazine (NF-κB inhibitor) both significantly inhibited TNF-α-induced human amylin promoter activation (Fig. 7c), suggesting that AP1 and NF-κB also mediate TNF-α-induced human amylin gene expression.…”

Section: Tnf-α Induces Murine Amylin Expressionmentioning

confidence: 96%

TNF-α acutely upregulates amylin expression in murine pancreatic beta cells

Cai

Wang

et al. 2010

Diabetologia

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Aims/hypothesis Amylin, a secretory protein mainly produced by pancreatic beta cells, is elevated in the circulation of patients with diseases related to acute and chronic inflammation, including acute pancreatitis, pancreas graft rejection, obesity and insulin resistance. TNF-α is involved in these disorders. We investigated the effect of TNF-α on amylin levels and the underlying mechanisms, using murine pancreatic beta cell line MIN6 and pancreatic islets. Methods Amylin, proinsulin and prohormone convertase 1/3, 2 (Pc1/3, Pc2 [also known as Pcsk1/3 and Pcsk2, respectively]) mRNA levels, and amylin promoter and nuclear factor κB (NF-κB) activation were examined by real-time PCR and luciferase reporter assay, respectively. Amylin protein level and mitogen-activated protein kinase phosphorylation were detected by western blot. Activator protein 1 (AP1) activation was examined by electrophoretic mobility shift assay (EMSA).Results TNF-α acutely induced amylin expression at the transcriptional level and increased proamylin and the intermediate form of amylin in MIN6 cells and islets. However, it had no effect on proinsulin, Pc1/3 and Pc2 expression. Studies with (1) MIN6 cells treated with inhibitors of MEK1/2, c-Jun-N-terminal kinase (JNK) or protein kinase CK PKC ð z Þ, (2) MIN6 cells expressing a c-Jun-dominant negative construct and (3) islets from Fos knockout mice demonstrated that TNF-α induced amylin expression through the PKC z Àextracellular signal-regulated kinase (ERK)/JNK pathways. EMSA showed that PKC z , JNK and ERK1/2 were involved in TNF-α-induced AP1 activation, suggesting that TNF-α induces murine amylin expression through the PKC z ÀERK1=2ÀAP1 and PKC z À JNKÀAP1 pathways. Further studies showed that TNF-α also induced murine amylin expression through the phosphatidylinositol 3 kinase-NF-κB signalling pathway and enhanced human amylin promoter activation through NF-κB and AP1. Conclusions/interpretation TNF-α acutely induces amylin gene expression in beta cells through multiple signalling pathways, possibly contributing to amylin elevation in acute inflammation-related pancreatic disorders.

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New and known symmetrical curcumin derivatives inhibit the formation of Fos-Jun-DNA complex

Cited by 60 publications

References 13 publications

Modulation of Differentiation-related Gene 1 Expression by Cell Cycle Blocker Mimosine, Revealed by Proteomic Analysis

Modulation of Differentiation-related Gene 1 Expression by Cell Cycle Blocker Mimosine, Revealed by Proteomic Analysis

Curcumin Inhibits Neurotensin-Mediated Interleukin-8 Production and Migration of HCT116 Human Colon Cancer Cells

TNF-α acutely upregulates amylin expression in murine pancreatic beta cells

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