EGCG-targeted p57/KIP2 reduces tumorigenicity of oral carcinoma cells: Role of c-Jun N-terminal kinase

Yamamoto, Tetsuya; Digumarthi, Hari; Aranbayeva, Zina; Wataha, John C.; Lewis, Jill B.; Messer, Regina L. W.; Qin, Haiyan; Dickinson, Douglas; Osaki, Tokio; Schuster, George S.; Hsu, Stephen

doi:10.1016/j.taap.2006.11.013

Cited by 28 publications

(22 citation statements)

References 45 publications

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“…Inhibition of MMP-2 and MMP-9 levels was also observed by the authors after treatment with EGCG (Kato et al, 2008). EGCG potently induces p57 in normal human primary epidermal keratinocytes, but not in epithelial cancer cells (Yamamoto et al, 2007). In humans, reduced expression of p57 is associated with advanced tumors, and tumor cells with inactivated p57 undergo apoptosis when exposed to EGCG (Yamamoto et al, 2007).…”

Section: Introductionsupporting

confidence: 53%

“…EGCG potently induces p57 in normal human primary epidermal keratinocytes, but not in epithelial cancer cells (Yamamoto et al, 2007). In humans, reduced expression of p57 is associated with advanced tumors, and tumor cells with inactivated p57 undergo apoptosis when exposed to EGCG (Yamamoto et al, 2007). In normal human primary epidermal keratinocytes, EGCGinduces p57 through the p38 mitogen-activated protein kinase signaling pathway (Yamamoto et al, 2007).…”

Section: Introductionmentioning

confidence: 99%

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Polyphenols as a chemopreventive agent in oral carcinogenesis

Moura¹,

Noguti²,

Jesus³

et al. 2013

European Journal of Cancer Prevention

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Polyphenols are present in foods and beverages, being related to sensorial qualities such as color, bitterness, and astringency, which are relevant in products such as wine, tea, and grape juice. These compounds occur naturally in forms varying from simple phenolic acids to complex polymerized tannins. Oral cancer is the most common head and neck cancer, and it often has a poor prognosis owing to local tumor invasion and frequent lymph node metastasis. Nowadays, chemoprevention is considered as a promising approach for controlling cancer as a result of specific natural products or synthetic agents able to suppress, reverse, or even prevent premalignancy before transformation into invasive cancer. The use of polyphenols as a chemopreventive agent is a suitable tool for modulation of the oral carcinogenesis process. The aim of this article is to present data generated from the use of polyphenols as a chemopreventive agent in oral carcinogenesis using in-vivo and in-vitro test systems. These results have shown that polyphenols are able to exert some chemopreventive action as a result of inducing cellular death, apoptosis, inhibition of tumor growth, and antioxidative properties. Therefore, this area warrants further investigation as a new approach that would apply not only to polyphenols but also to other phytochemicals used as promising therapeutic agents against oral human diseases, especially cancer.

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Section: Introductionsupporting

confidence: 53%

Section: Introductionmentioning

confidence: 99%

Polyphenols as a chemopreventive agent in oral carcinogenesis

Moura¹,

Noguti²,

Jesus³

et al. 2013

European Journal of Cancer Prevention

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“…Equally, while GILZ did not show significant enhancement by LABAs Rider et al, 2011), the effect of glucocorticoid plus LABA on MKP-1 is additive Manetsch et al, 2012). Other genes, for example p57 KIP2 (CDKN1C), a cell cycle regulator that is implicated in inhibition of the c-Jun Nterminal kinase MAPK pathway (Chang et al, 2003;Yamamoto et al, 2007), show enhancement of glucocorticoid-driven transcription by LABAs Rider et al, 2011). Taken with the current data for RGS2, this illustrates how combining a LABA with an ICS could produce superior clinical benefits when compared with each monotherapy.…”

Section: Rgs2 Expression In Bronchial Epithelial Cellsmentioning

confidence: 98%

Induction of Regulator of G-Protein Signaling 2 Expression by Long-Acting β₂-Adrenoceptor Agonists and Glucocorticoids in Human Airway Epithelial Cells

Holden

George

Rider

et al. 2013

J Pharmacol Exp Ther

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In asthma and chronic obstructive pulmonary disease (COPD) multiple mediators act on Ga q -linked G-protein-coupled receptors (GPCRs) to cause bronchoconstriction. However, acting on the airway epithelium, such mediators may also elicit inflammatory responses. In human bronchial epithelial BEAS-2B cells (bronchial epithelium 1 adenovirus 12-SV40 hybrid), regulator of G-protein signaling (RGS) 2 mRNA and protein were synergistically induced in response to combinations of long-acting b 2 -adrenoceptor agonist (LABA) (salmeterol, formoterol) plus glucocorticoid (dexamethasone, fluticasone propionate, budesonide). Equivalent responses occurred in primary human bronchial epithelial cells. Concentrations of glucocorticoid plus LABA required to induce RGS2 expression in BEAS-2B cells were consistent with the levels achieved therapeutically in the lungs. As RGS2 is a GTPase-activating protein that switches off Ga q , intracellular free calcium ([Ca 21 ] i ) flux was used as a surrogate of responses induced by histamine, methacholine, and the thromboxane receptor agonist U46619. This was significantly attenuated by salmeterol plus dexamethasone pretreatment, or RGS2 overexpression, and the protective effect of salmeterol plus dexamethasone was abolished by RGS2 RNA silencing. Although methacholine and U46619 induced interleukin-8 (IL-8) release and this was inhibited by RGS2 overexpression, the repression of U46619-induced IL-8 release by salmeterol plus dexamethasone was unaffected by RGS2 knockdown. Given a role for Ga q -mediated pathways in inducing IL-8 release, we propose that RGS2 acts redundantly with other effector processes to repress IL-8 expression. Thus, RGS2 expression is a novel effector mechanism in the airway epithelium that is induced by glucocorticoid/LABA combinations. This could contribute to the efficacy of glucocorticoid/LABA combinations in asthma and COPD.

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“…This allows p57 Kip2 to interact with PCNA, although with a much lower affinity compared with p21 Cip1 , and in turn block processive DNA synthesis (46). In addition, the p57 Kip2 QT domain interacts with and inhibits the kinase activity of c-Jun NH2-terminal kinase/stress-activated protein kinase [JNK/SAPK (47,48)]. Of interest, p21 Cip1 is also able to bind and suppress JNK/SAPK activity via its amino-terminal domain.…”

Section: P57 Kip2 Proteinmentioning

confidence: 99%

p57Kip2 and Cancer: Time for a Critical Appraisal

Borriello

Caldarelli

Bencivenga

et al. 2011

Molecular Cancer Research

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p57Kip2 is a cyclin-dependent kinase inhibitor belonging to the Cip/Kip family, which also includes p21Cip1 and p27Kip1. So far, p57Kip2 is the least-studied Cip/Kip protein, and for a long time its relevance has been related mainly to its unique role in embryogenesis. Moreover, genetic and molecular studies on animal models and patients with Beckwith-Wiedemann syndrome have shown that alterations in CDKN1C (the p57Kip2 encoding gene) have functional relevance in the pathogenesis of this disease. Recently, a number of investigations have identified and characterized heretofore unexpected roles for p57Kip2. The protein appears to be critically involved in initial steps of cell and tissue differentiation, and particularly in neuronal development and erythropoiesis. Intriguingly, p27Kip1, the Cip/Kip member that is most homologous to p57Kip2, is primarily involved in the process of cell cycle exit. p57Kip2 also plays a critical role in controlling cytoskeletal organization and cell migration through its interaction with LIMK-1. Furthermore, p57Kip2 appears to modulate genome expression. Finally, accumulating evidence indicates that p57Kip2 protein is frequently downregulated in different types of human epithelial and nonepithelial cancers as a consequence of genetic and epigenetic events. In summary, the emerging picture is that several aspects of p57Kip2's functions are only poorly clarified. This review represents an appraisal of the data available on the p57Kip2 gene and protein structure, and its role in human physiology and pathology. We particularly focus our attention on p57Kip2 changes in cancers and pharmacological approaches for modulating p57Kip2 levels. Mol Cancer Res; 9(10); 1269–84. ©2011 AACR.

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EGCG-targeted p57/KIP2 reduces tumorigenicity of oral carcinoma cells: Role of c-Jun N-terminal kinase

Cited by 28 publications

References 45 publications

Polyphenols as a chemopreventive agent in oral carcinogenesis

Polyphenols as a chemopreventive agent in oral carcinogenesis

Induction of Regulator of G-Protein Signaling 2 Expression by Long-Acting β₂-Adrenoceptor Agonists and Glucocorticoids in Human Airway Epithelial Cells

p57Kip2 and Cancer: Time for a Critical Appraisal

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EGCG-targeted p57/KIP2 reduces tumorigenicity of oral carcinoma cells: Role of c-Jun N-terminal kinase

Cited by 28 publications

References 45 publications

Polyphenols as a chemopreventive agent in oral carcinogenesis

Polyphenols as a chemopreventive agent in oral carcinogenesis

Induction of Regulator of G-Protein Signaling 2 Expression by Long-Acting β2-Adrenoceptor Agonists and Glucocorticoids in Human Airway Epithelial Cells

p57Kip2 and Cancer: Time for a Critical Appraisal

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Induction of Regulator of G-Protein Signaling 2 Expression by Long-Acting β₂-Adrenoceptor Agonists and Glucocorticoids in Human Airway Epithelial Cells