Signal transducers and activators of transcription—from cytokine signalling to cancer biology

Santos, Carlos Pereira dos; Costa-Pereira, Ana P.

doi:10.1016/j.bbcan.2011.03.003

Cited by 48 publications

(51 citation statements)

References 231 publications

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“…The binding of a cytokine to its cell-surface receptor results in the activation of JAK tyrosine kinases, which in turn phosphorylate STATs. Then, STATs dimerize, translocate into the nucleus and activate the transcription of STAT-responsive genes, namely iNOS [42][43][44][45]. The present study demonstrated, for the first time, that pre-incubation of C3G in HT-29 cells decreased the nuclear levels of this activated transcription factor, to about 50% ( Figure 7).…”

Section: Discussionmentioning

confidence: 64%

Cyanidin-3-glucoside suppresses cytokine-induced inflammatory response in human intestinal cells: comparison with 5-aminosalicylic acid

Serra¹,

Paixão²,

Nunes³

et al. 2012

Free Radical Biology and Medicine

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The potential use of polyphenols in the prevention and treatment of chronic inflammatory diseases has been extensively investigated although the mechanisms involved in cellular signaling need to be further elucidated. Cyanidin-3-glucoside is a typical anthocyanin of many pigmented fruits and vegetables widespread in the human diet. In the present study, the protection afforded by cyanidin-3-glucoside against cytokine-triggered inflammatory response was evaluated in the human intestinal HT-29 cell line, in comparison with 5-aminosalicylic acid, a well-established anti-inflammatory drug, used in inflammatory bowel disease. For this purpose, some key inflammatory mediators and inflammatory enzymes were examined. Our data showed that cyanidin-3-glucoside reduced cytokine-induced inflammation in intestinal cells, in terms of NO, PGE 2 and IL-8 production and of iNOS and COX-2 expressions, at a much lower concentration than 5-aminosalicylic acid, suggesting a higher anti-inflammatory efficiency. Interestingly, cyanidin-3-glucoside and 5-aminosalicylic acid neither prevented IkB-a degradation nor the activation of NF-kB, but significantly reduced cytokine-induced levels of activated STAT1 accumulated in the cell nucleus. In addition, we established that phosphorylated p38 MAPK was not involved in the protective effect of cyanidin-3-glucoside or 5-aminosalicylic acid. Taking into account the high concentrations of dietary anthocyanins potentially reached in the gastrointestinal tract, cyanidin-3-glucoside may be envisaged as a promising nutraceutical giving complementary benefits in the context of inflammatory bowel disease.

show abstract

Section: Discussionmentioning

confidence: 64%

Cyanidin-3-glucoside suppresses cytokine-induced inflammatory response in human intestinal cells: comparison with 5-aminosalicylic acid

Serra¹,

Paixão²,

Nunes³

et al. 2012

Free Radical Biology and Medicine

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“…OSM and IL-6 are both members of the gp130 family (9,10) and utilize the JAK-STAT signaling pathway to effect downstream cellular events (11,12). Upon cytokines binding to their cell surface receptors, the tyrosine kinase JAK becomes activated and phosphorylates the STAT molecules associated with the receptor tail.…”

mentioning

confidence: 99%

“…The phosphorylated STAT molecules form dimers and then translocate to the nucleus where they bind to the promoters of their target genes to regulate transcription. A wide range of cellular processes are controlled by the JAK-STAT pathway through transcriptional regulation of STAT target genes in response to various cytokines and growth factors (11,12). One member of the STAT family, STAT3, is specifically activated by the gp130 family of cytokines, including IL-6 and OSM (9,10).…”

mentioning

confidence: 99%

Signal Transducers and Activators of Transcription 3 (STAT3) Directly Regulates Cytokine-induced Fascin Expression and Is Required for Breast Cancer Cell Migration

Snyder

Huang

Zhang

2011

Journal of Biological Chemistry

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Background:The goal is to understand the molecular mechanism of metastasis and the roles of IL-6/OSM, STAT3, and fascin. Results: STAT3 binds to the fascin promoter and is essential for its expression and cell migration in response to IL-6/OSM. Conclusion: STAT3 plays a central role in cell migration through direct control of fascin expression. Significance: Drug targets are identified to block tumor metastasis.

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“…The STAT (signal transducers and activators of transcription) proteins are a family of transcription factors that play various roles in cellular processes, including immune response, apoptosis, and oncogenesis (1)(2)(3)(4). STATs are members of the JAK-STAT signaling pathway, which is activated by growth factors and cytokines (1,2).…”

mentioning

confidence: 99%

A Signal Transducer and Activator of Transcription 3·Nuclear Factor κB (Stat3·NFκB) Complex Is Necessary for the Expression of Fascin in Metastatic Breast Cancer Cells in Response to Interleukin (IL)-6 and Tumor Necrosis Factor (TNF)-α

Snyder

Huang

et al. 2014

Journal of Biological Chemistry

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Background: IL-6/Stat3 promote breast cancer metastasis through regulation of the fascin gene. Results: In addition to IL-6, TNF-␣ induces binding of a Stat3⅐NFB complex to the fascin promoter to induce transcription. Conclusion: Both NFB and Stat3 are required for cytokine-induced fascin expression and cell migration. Significance: Identification of proteins critical for breast cancer metastasis will reveal drug targets.

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Signal transducers and activators of transcription—from cytokine signalling to cancer biology

Cited by 48 publications

References 231 publications

Cyanidin-3-glucoside suppresses cytokine-induced inflammatory response in human intestinal cells: comparison with 5-aminosalicylic acid

Cyanidin-3-glucoside suppresses cytokine-induced inflammatory response in human intestinal cells: comparison with 5-aminosalicylic acid

Signal Transducers and Activators of Transcription 3 (STAT3) Directly Regulates Cytokine-induced Fascin Expression and Is Required for Breast Cancer Cell Migration

A Signal Transducer and Activator of Transcription 3·Nuclear Factor κB (Stat3·NFκB) Complex Is Necessary for the Expression of Fascin in Metastatic Breast Cancer Cells in Response to Interleukin (IL)-6 and Tumor Necrosis Factor (TNF)-α

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